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Breast cancer (BC) is one of the most common malignant cancers in females worldwide and greatly threatens women's health. The C-type lectin domain family 10 member A (CLEC10A) is a member of the C-type lectin receptor family that has been previously reported to promote the antitumor activity of immune cells. In the present study, the potential prognostic value of CLEC10A expression in BC was assessed using data from The Cancer Genome Atlas online database. Differences in the mRNA expression levels of CLEC10A between BC and normal tissues were then analyzed using the Tumor Immune Estimation Resource (TIMER) platform and the University of Alabama at Birmingham Cancer data analysis portal. Reverse transcription-quantitative PCR was performed to validate the results of this analysis. The Kaplan-Meier plotter database was used to evaluate the association between the mRNA expression levels of CLEC10A and clinical prognosis of BC. Based on the association between the mRNA expression levels of CLEC10A and the tumor immune microenvironment, the TIMER platform and the Tumor and Immune System Interaction Database website were utilized to assess the correlation between CLEC10A expression and the degree of tumor immune cell infiltration. The present study revealed that CLEC10A expression was significantly lower in BC tissues compared with that in normal tissues, which was in turn associated with poorer clinical outcomes. This suggested that lower CLEC10A expression levels were associated with unfavorable prognosis in BC. In addition, the expression level of CLEC10A was found to be positively associated with the level of different tumor-infiltrating immune cells in BC, including CD8 T cells, B cells, macrophages and NK cells which, was in turn closely correlated with some gene markers such as CD19, CD8A, KIR2DS4 and PTGS2. These results suggest that the relationship between lower CLEC10A expression level and poor prognosis in BC may be due to the role of CLEC10A in the tumor immune microenvironment. In conclusion, CLEC10A may be a potential biomarker that can be used to efficiently predict prognosis in patients with BC.

Preeclampsia (PE) is characterized by gestational hypertension and proteinuria, and is a leading cause of maternal death and perinatal morbidity globally. Although the exact cause of PE remains unclear, several studies have suggested a role for abnormal expression of multiple genes. The aim of the present study was to identify key genes and related pathways, and to screen for drugs that regulate these genes for potential PE therapy. The GSE60438 dataset was acquired from the Gene Expression Omnibus database to analyze differentially expressed genes (DEGs). By constructing a protein-protein interaction network and performing reverse transcription-quantitative PCR verification, proteasome 26S subunit, non-ATPase 14, prostaglandin E synthase 3 and ubiquinol-cytochrome c reductase core protein 2 were identified as key genes in PE. In addition, PE was found to be associated with ‘circadian rhythm’, ‘fatty acid metabolism’, ‘DNA damage response detection of DNA damage’, ‘regulation of DNA repair’ and ‘endothelial cell development’. Through connectivity map analysis of DEGs, furosemide and droperidol were suggested to be therapeutic drugs that may target the hub genes for PE treatment. Results analysis of GSEA were included in the discussion section of this article. In conclusion, the current study identified novel key genes associated with the onset of PE and potential drugs for PE treatment.

Macrophages are a heterogeneous group of phagocytes that play critical roles in inflammation, infection and tumor growth. Macrophages respond to different environmental factors and are thereby polarized into specialized functional subsets. Although hypoxia is an important environmental factor, its impact on human macrophage polarization and subsequent modification of the inflammatory microenvironment have not been fully established. The present study aimed to elucidate the effect of hypoxia exposure on the ability of human macrophages to polarize into the classically activated (pro-inflammatory) M1, and the alternatively activated (anti-inflammatory) M2 phenotypes. The effect on the inflammatory microenvironment and the subsequent modification of A549 lung carcinoma cells was also investigated. The presented data show that hypoxia promoted macrophage polarization towards the M2 phenotype, and modified the inflammatory microenvironment by decreasing the release of proinflammatory cytokines. Modification of the microenvironment by proinflammatory M1 macrophages under hypoxia reversed the inhibition of malignant behaviors within the proinflammatory microenvironment. Furthermore, it was identified p38 signaling (a major contributor to the response to reactive oxygen species generated by hypoxic stress), but not hypoxia-induced factor, as a key regulator of macrophages under hypoxia. Taken together, the data suggest that hypoxia affects the inflammatory microenvironment by modifying the polarization of macrophages, and thus, reversing the inhibitory effects of a proinflammatory microenvironment on the malignant behaviors of several types of cancer cell.

Research suggests that daphnoretin exhibits a diverse array of antitumor mechanisms and pharmacological activities. However, there is no definitive explanation for the antitumor mechanisms of daphnoretin in malignant melanoma. In the present study, MTT and colony formation assays demonstrated that daphnoretin significantly inhibited the proliferation of melanoma A375 and B16 cells. Following treatment with daphnoretin, apoptotic bodies were observed in A375 and B16 cells via Hoechst 33258 staining. Furthermore, western blot analysis revealed that the apoptosis-related proteins cleaved caspase-3, cleaved caspase-9, Bax, cytochrome c and apoptotic protease-activating factor 1 were significantly upregulated, while the expression levels of caspase-3, caspase-9 and Bcl-2 were downregulated in A375 and B16 cells. Flow cytometry and fluorescence microscopy revealed that daphnoretin induced higher levels of reactive oxygen species (ROS). Therefore, the results of the present study indicated that daphnoretin induced ROS-mediated mitochondria apoptosis in human (A375) and murine (B16) malignant melanoma cells.

Esophageal cancer is one of the most common types of malignancy worldwide. At present, surgical resection is the main treatment for esophageal cancer, but recurrence and distant metastasis are the main causes of mortality. The transcription factors Twist, Slug and Snail regulate epithelial-mesenchymal transition and thereby participate in tumor invasion and metastasis. The aim of the present study was to investigate the expression of Twist, Slug and Snail in esophageal squamous cell carcinoma (ESCC) and their prognostic significance. The expression of Twist, Slug and Snail in 229 paraffin-embedded ESCC and matched normal mucosal tissues was detected by immunohistochemistry. The expression differences of Twist, Slug and Snail in the ESCC and normal tissues were compared by χ2 test, and the associations between the three proteins and the clinicopathological parameters of ESCC were analyzed. The expression levels of Twist, Slug and Snail in 29 fresh frozen ESCC and matched normal mucosal tissues were detected by reverse transcription-quantitative PCR. The correlations among Twist, Slug and Snail in ESCC were examined by Pearson's correlation analyses. In addition, single factor and multivariate Cox regression analyses were used to analyze the influence of Twist, Slug and Snail on the prognosis of ESCC. Twist was found to be highly expressed in ESCC. The difference of Slug expression in ESCC was associated with differentiation degree, TNM stage and vascular invasion, but no significant association was observed between Snail expression and any clinicopathological parameters. In ESCC, there were significant differences in protein expression between Twist and Snail, and Slug and Snail. The mRNA expression level of Twist in ESCC was significantly higher than that in normal esophageal mucosa. However, the mRNA expression of Slug in normal esophageal mucosa was higher than that in ESCC, and the mRNA expression levels of Twist and Snail were positively correlated in ESCC. Kaplan-Meier analysis of 229 patients with ESCC revealed that Snail influenced the overall survival, as did the co-expression of Twist and Snail. Nerve invasion was also identified as an independent factor affecting the progression-free survival of ESCC. The results indicate that Twist is highly expressed, Slug may be a tumor suppressor, and Snail is an independent prognostic factor in ESCC. Twist and Snail are positively correlated, and the simultaneous inhibition of Twist and Snail protein expression may be beneficial for prolonging the overall survival of patients with ESCC.

Long non-coding (lnc)RNAs have been recognized as important regulators in gastric cancer. lncRNA GAS8-AS1 is considered a tumor suppressor in multiple types of cancer, such as papillary thyroid carcinoma, ovarian cancer and colorectal cancer. However, the specific role of GAS8-AS1 in gastric cancer remains to be fully elucidated. The aim of the present study was to investigate the role of GAS8-AS1 in gastric cancer and its potential underlying mechanisms of action. The expression levels of GAS8-AS1, microRNA (miR)-21-3p, PTEN and pyruvate dehydrogenase (E1) alpha subunit gene (PDHA1) in gastric cancer and non-cancerous tissues, as well as in gastric cancer cell lines, were detected using reverse transcription-quantitative PCR. Cell proliferation was detected by using a Cell Counting Kit-8 assay. Cell migration and invasion were detected using a Transwell assay. Results of the present study demonstrated that the expression levels of GAS8-AS1 in gastric cancer tissues were significantly decreased, whereas its expression did not differ among cancer tissues at different clinical stages. Low expression levels of GAS8-AS1 predicted poor 5-year survival rates for 70 patients with gastric adenocarcinoma from the Affiliated Hospital of Xuzhou Medical University (Xuzhou, China) during patient follow-up. In addition, the expression levels of miR-21-3p were markedly increased in cancer tissues, and miR-21-3p expression was negatively associated with the expression of GAS8-AS1. The direct interaction between GAS8-AS1 and miR-21-3p was predicted using the starBase database and was confirmed by using an RNA pull-down assay. In gastric cell lines, the overexpression of GAS8-AS1 reduced the expression levels of mature miR-21-3p but did not affect the expression of miR-21-3p precursor, while the overexpression of miR-21-3p did not, in turn, affect the expression of GAS8-AS1. In addition, the overexpression of GAS8-AS1 inhibited cancer cell proliferation, while the overexpression of miR-21-3p promoted cancer cell proliferation and attenuated the effects of GAS8-AS1. Overexpression of miR-21-3p promoted cancer cell migration and invasion, whereas overexpression of GAS8-AS1 did not affect cell migration or invasion. In summary, results of the present study have demonstrated that GAS8-AS1 acts as a tumor suppressor in gastric cancer, and it may inhibit cancer cell proliferation by downregulating miR-21-3p.

Early detection of nasopharyngeal carcinoma (NPC) is of vital importance for improving prognosis and survival rates. MicroRNA (miRNA) are a class of short and non-coding RNA molecules that are capable of inhibiting the translation of mRNA of target genes. Previous studies have revealed that miRNA are involved in tumorigenesis and cancer development. The RNase-resistance of circulating miRNA have made them valuable non-invasive biomarkers, and has therefore drawn particular attention to their therapeutic potential. The aim of the present study was to investigate the expression of the previously uncharacterized miR-639 in NPC. In a study population of 139 patients, higher expression of miR-639 was associated with metastasis, more advanced cancer stages, and lower disease-free survival rates. In vitro experiments involving transfection of human NPC C666-1 and NPC/HK1 cell lines with miR-639 mimics and antagomir indicated that overexpressing miR-639 promoted cell proliferation and migration, suppression of miR-639 inhibited proliferation and migration. The present study provides evidence that miR-639 is differentially expressed in NPC tissues of varying cancer stages, and suggests that quantifying circulating miR-639 may be of importance for non-invasive diagnosis and prognostic evaluation, and may have potential therapeutic utility.

Proline-rich tyrosine kinase 2 (Pyk2), a member of the focal adhesion kinase family, has recently been associated with tumor development. However, the role of Pyk2 in renal cell carcinoma (RCC) remains unexplored. The present study investigated the expression pattern, clinical significance, and function of Pyk2 in RCC. By using a reverse transcription-quantitative polymerase chain reaction, tissue microarray and immunohistochemistry, it was demonstrated that RCC tissues display a higher Pyk2 expression compared with paired adjacent nontumor tissues. Furthermore, it was revealed that Pyk2 upregulation was associated with poor clinical outcomes in patients with RCC. By using loss-of-function approaches, it was demonstrated that Pyk2 knockdown reduced cell viability, invasive ability and migratory ability, and increased apoptosis in RCC cell lines. In contrast, Pyk2 overexpression promoted tumor cell proliferation, invasion and migration and reduced apoptosis. Collectively, the results of the present study present the tumor-promoting function of Pyk2 in RCC and thus provide molecular evidence for novel tyrosine kinase inhibitors as novel therapeutic options for RCC.

Lung adenocarcinoma (LA) is a common non-small cell lung cancer, but effective biomarkers to diagnose early LA are still lacking. Increasing evidence has indicated that the dysregulation of microRNAs (miRNAs) play crucial roles in LA progression. miR-339-5p has been recently confirmed to exert crucial functions in various cancers. Nevertheless, molecular mechanisms and effects of miR-339-5p on LA development still remain vague. In the present research, miR-339-5p expression was downregulated in human LA tissues. miR-339-5p overexpression in LA cells could remarkably suppress the LA cell invasion and migration. In addition, further studies indicated that miR-339-5p overexpression downregulated both the B-cell lymphoma 6 (BCL6) mRNA and protein expressions by targeting the BCL6 3'-UTR directly. Moreover, BCL6 knockdown could partially lessen the function of miR-339-5p in LA invasion and migration. In conclusion, the present data identified miR-339-5p as a novel LA suppressor which exerted its functions partly by negatively regulating BCL6.

Mucinous adenocarcinoma is an unusual histological type of lung cancer, and its clinicopathological feature is distinctive from that of other histopathological types of lung adenocarcinoma. Mucinous adenocarcinoma has a mucus-producing function, which explains its name. The present study reports a rare case of a mucus-producing adenocarcinoma of the lung. A 60-year-old Chinese female patient was diagnosed with mucinous adenocarcinoma of the lung, which manifested as respiratory symptoms, including fever, cough and expectoration. The patient received thoracic exploratory operation and right pneumonectomy, since the above respiratory symptoms seriously affected her daily life, and other inspections could not establish the diagnosis. Histopathology revealed no mutations in epidermal growth factor receptor. The patient received adjuvant chemotherapy using taxol and cisplatin. However, metastases in the left lung were detected 7 months after the operation. Pemetrexed and cisplatin were used as the second-line treatment. The patient survived 3 years after the initial diagnosis. The present study reports a rare mucus-producing adenocarcinoma of the lung, which is of bad prognosis. Therefore, further studies on this type of cancer are urgently required.

Promoter hypermethylation of tumor suppressor genes has been confirmed to serve a pivotal role in tumorigenesis. Protocadherin 8 (PCDH8), a novel tumor suppressor gene, has been reported to be inactivated by promoter hypermethylation a number of cancer types, including bladder cancer and renal cell carcinoma. The aim of the present study was to investigate the occurrence of PCDH8 hypermethylation in prostate cancer and its potential as a novel biomarker of prostate cancer. The transcriptional levels of PCDH8 were examined by quantitative polymerase chain reaction (PCR) in 82 prostate cancer tissues as well as 30 prostate hyperplasia tissues, and verified the protein level by western blot analysis of representative samples. PCDH8 expression levels were found to be reduced to 0.30±0.10 in 70.7% (58/82) of prostate cancer tissues. To identify the possible reason for mRNA downregulation, the methylation status of the PCDH8 promoter was assessed in prostate cancer tissues and prostate hyperplasia tissues by methylation-specific PCR (MSP). A total of 47 prostate cancer patients who exhibited reduced PCDH8 expression (57.3%; 47/82) also showed promoter hypermethylation (47/58). None of the samples (0/30) in the benign prostate hyperplasia group were positive on MSP. Furthermore, the associations between the methylation status of the PCDH8 promoter and various clinicopathological features of prostate cancer were analyzed, revealing that the methylation status of PCDH8 was closely associated with tumor size, tumor shape (papillary/non-papillary), tumor stage and tumor grade (all P0.05). Additionally, patients with hypermethylation of the PCDH8 gene promoter had a relapse rate of 36.17% and a mortality rate of 29.79%, which were significantly higher than the hypermethylation-negative patients (P

Although a combination of platinum- and taxane-based chemotherapy is recommended for at least 70% patients with ovarian cancer as treatment subsequent to surgery, the initial response to the chemotherapy is not durable and tumors become resistant. Histone deacetylase and proteasome inhibitors are novel therapeutic agents. However, the moderate antitumoral effect of the inhibitors has restricted their clinical use when used as single agents. The aim of the present study was to investigate the synergistic activity of trichostatin A (TSA) and PS-341 in ovarian cancer cells, along with the investigation of the molecular mechanisms of taxane resistance. The taxane-sensitive ovarian cancer A2780 cell line and its resistant variant, A2780T, were treated with taxane, TSA and PS-341 at various concentrations. An Annexin V assay was performed to determine the levels of cell viability and apoptosis, while flow cytometry and immunofluorescence staining for the mitotic phase-specific protein phosphorylated-histone H3 (Ser10) were used for cell cycle detection. The effects of combined TSA and PS-341 on cell cycle-associated proteins were tested by western blot analysis. Furthermore, the present study examined the apoptosis and cell cycle arrest induced by the 3 agents subsequent to overexpression or downregulation of cyclin B1 in A2780 and A2780T cells, respectively. It was found that TSA interacted synergistically with PS-341, resulting in a marked increase in apoptosis and the rate of G2/M arrest in A2780T cells. A lower basal level of cyclin B1 expression and the incompetence of the upregulation of the cyclin may explain the taxane resistance found in A2780T cells. Collectively, the combination of TSA and PS-341 increased cyclin B1 expression level regardless of the basal expression level, resulting in the proliferation inhibition and apoptosis in A2780 and A2780T cells, which raised the possibility that a combination of the two drugs may represent a novel strategy for the treatment of ovarian cancer, particularly in taxane-resistant ovarian cancer.

In the majority of acute promyelocytic leukemia (APL) cases, translocons produce a promyelocytic leukemia protein-retinoic acid receptor α (PML-RARα) fusion gene. Studies have reported that neutrophil elastase (NE) cleaves bcr-1-derived PML-RAα in early myeloid cells, leaving only the nuclear localization signal (NLS) of PML attached to RARα. NLS-RARα promotes cell growth and inhibits differentiation in response to ATRA. However, the mechanisms by which NLS-RARα affects cell biological characteristics are yet to be fully elucidated. The present study found that the location of RARαwas altered after it was cleaved by NE. Firstly, NE was overexpressed during the preparation of recombinant plasmid NB-4/pCMV6-NE-Myc to cleave PML-RARα. The total protein expression levels of myc and NE and expression levels of NLS-RARα in nucleoprotein were detected by western blotting. Location of NLS-RARα protein was detected by immunofluorescence and confocal laser scanning. Secondly, a nude mice model was constructed and NE protein, NLS-RARα and RARα protein assays, and the location of NLS-RARα and RARα proteins were assessed as described. The present results showed that, compared with the control groups, the location of NLS-RARα protein was predominantly detected in the nucleus, whereas RARα was mainly distributed in the cytoplasm. These findings were consistent with those of the nude mice model, and these may be used as a foundation to explain the occurrence mechanism of APL.

A component purified from Strongylocentrotus nudus eggs on a diethylaminoethyl cellulose-52 chromatography column and eluted using a NaCl solution gradient (SEP-S), is a homogeneous polysaccharide of α-D-glucan with a reduced molecular weight of 9.33×105 Da, compared with that of S. nudus egg polysaccharide (SEP). In an in vivo antitumor assay of histocompatibility-22 hepatocellular carcinoma in tumor-bearing mice, the inhibitory rates at SEP-S doses of 5, 10 and 20 mg/kg/day were 38.8, 50.7 and 70.3%, respectively. In addition, the spleen and thymus indices and the percentages of cluster of differentiation (CD) 4+ and CD8+ T cells were significantly increased, and the activity of cytotoxic T lymphocytes was notably enhanced, suggesting that the anti-hepatocellular carcinoma activity is mediated by boosting the immune system. In vitro experiments also demonstrated that splenocyte proliferation induced by SEP-S was inhibited by the toll-like receptor (TLR) 2 and TLR4 monoclonal antibodies. These data indicate that SEP-S is a polysaccharide component possessing high anti-hepatocellular carcinoma activity and may be a potential immunotherapy candidate for the treatment of liver cancer.

The aim of the present study was to examine the function of long intergenic non-protein coding RNA 1638 (LINC01638) long non-coding RNA (lncRNA) in hepatocellular carcinoma (HCC). In the present study, gene expression was analyzed using qPCR and western blotting. Glucose uptake was analyzed using a glucose uptake assay and cell proliferation was analyzed using a cell counting kit-8 assay. LINC01638 lncRNA and glucose transporter 1 (GLUT1) were upregulated in tumor tissues compared with adjacent healthy tissues of patients with HCC. Expression levels of LINC01638 lncRNA and GLUT1 were positively correlated only in tumor tissues; however, there was no correlation in adjacent healthy tissues. Overexpression of LINC01638 lncRNA and GLUT1 promoted glucose uptake, while LINC01638 lncRNA and GLUT1-knockdown led to inhibited glucose uptake of cells of HCC cell lines. Overexpression of LINC01638 lncRNA mediated the upregulation of GLUT1 expression and accelerated cell proliferation. GLUT1 overexpression failed to significantly affect LINC01638 lncRNA expression, however also promoted cancer cell proliferation. In addition, GLUT1-knockdown attenuated the effects of LINC01638 overexpression on cancer cell proliferation. Therefore, LINC01638 lncRNA promoted cancer cell proliferation in HCC, potentially by increasing cancer cell glucose uptake.

The aim of the present study was to predict the prognostic value of 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) in the metastatic lymph nodes (mLNs) of patients with papillary thyroid carcinoma (PTC) with a negative iodine-131 (131I) whole-body scan (WBS). The present retrospective study included 32 patients with PTC undergoing standard surgery and radioiodine treatment. All patients received 18F-FDG PET/CT imaging prior to and following therapy. All mLNs were divided into an effective treatment group (group A) and ineffective treatment group (group B) based on the PET Response Criteria in Solid Tumors 1.0 guidelines. All the patients were followed up for ≥9 months. A significant difference was identified in the peak standardized uptake value (SULpeak) between group B (7.85±3.20) and group A (5.36±2.19). A cut-off value of 5.85 was used to distinguish ineffective treatment of lesions from mLNs receiving radioactive ablation based on receiver operating characteristic (ROC) curve analysis with an area under the ROC curve of 0.755. Patients with a high SULpeak (P=0.003) and extrathyroidal extension (P=0.030), confirmed by pathology, more frequently exhibited a poor prognosis. In conclusion, tracer uptake of 18F-FDG for cervical metastatic nodes was revealed as a predictor for the clinical outcome of patients with PTC treated with radioiodine therapy. The present results also indicated that high SULpeak and extrathyroidal extension are poor predictors for patients with mLNs receiving 131I therapy.

Application value of nursing intervention combined with early nutritional support treatment in preventive stoma reversion of low rectal cancer was explored. Ninety-two cases of low rectal cancer patients undergoing preventive stoma reversion from January 2014 to December 2016 were retrospectively analyzed. All the patients had closed fistula 3 months after neostomy. Forty-four cases with routine nursing care were the control group; 48 cases with early nutritional support and nursing intervention were the experimental group. Nutritional status, psychological status, incidence of adverse reactions, wound infection rate, number of shaped and regular defecation were compared in the two groups. The levels of albumin, prealbumin and serum total protein in the experimental group were significantly higher than those in the control group after operation (P

Fatty acid metabolism is closely associated with the occurrence and development of tumors. The aim of the present study was to investigate whether the key enzyme involved in fatty acid synthesis, fatty acid synthase (FASN), mediates fatty acid changes that affect the activity and migration of breast cancer cells, and whether specific fatty acids play a role in tumor metastasis. The difference in serum fatty acid profiles between patients with invasive ductal carcinoma (IDC) and healthy controls was evaluated by gas chromatography-mass spectrometry (GC-MS) fatty acid profile analysis, and it was revealed that five types of fatty acids may be potential tumor markers in IDC. Immunohistochemistry and GC-MS analysis revealed that FASN expression affected the serum fatty acid profiles of patients with IDC. Following FASN knockdown, the migration of SK-Br-3 breast cancer cells was inhibited, and the contents of various fatty acids both inside and outside the cell decreased, while the contents of various fatty acids inside and outside the cell increased following FASN overexpression. The results of the present study revealed that the expression level of FASN affected the content of fatty acids in IDC tissues and breast cancer cell lines, and that FASN-mediated changes in specific fatty acids promoted tumor cell migration.

The objective of the present study was to investigate whether cyclooxygenase-2 (COX-2) is associated with malignancy, and to investigate its molecular mechanisms in human lung cancer tumor malignancy. The present study used RNA interference (RNAi) methodology and celecoxib, a COX-2 inhibitor, to investigate the effect of COX-2 knockdown on the proliferation and invasion abilities of lung cancer cells and the molecular mechanisms involved. Human lung adenocarcinoma A549-si10 and LTEP-A2 cells transfected with a specific small interfering RNA (A549-si10 and LTEP-A2-si10, respectively) grew more slowly compared with parental cell lines and cells transfected with pU6. The colony formation of A549-si10 and LTEP-A2-si10 cells was also reduced. In addition, A549-si10 and LTEP-A2-si10 cells were characterized by decreased metastatic and invasive abilities. The proliferation and invasive potential of parental A549 and LTEP-A2 cells was inhibited following treatment with celecoxib. In vivo, a COX-2 knockdown resulted in a decrease of proliferation and reduction of vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2) and endothelial growth factor receptor (EGFR) expression in A549 xenografts. In conclusion, the present study revealed that COX-2 plays a extremely important role in tumor growth, infiltration and metastasis via the regulation of VEGF, MMP-2 and EGRF expression. Therefore, COX-2 is a potential therapeutic target for lung cancer.

Tumor-like hypophysitis is an uncommon sellar condition that presents as inflammatory lesions on the structures of the pituitary gland. The diagnosis and management of hypophysitis poses a significant challenge, as its clinical manifestation and appearance in imaging studies are difficult to distinguish from that of pituitary tumors. The present retrospective study summarizes two rare cases of primary granulomatous hypophysitis, two cases of lymphocytic hypophysitis, and three cases in which a pathological diagnosis was not determined due to the use of hormone replacement therapy only. The mean age of the patients studied was 45.71±22.16 years, and the patients comprised two males and five females. The clinical signs of hypophysitis included headache, fever, gradual decrease in visual acuity, nausea and vomiting. Enhanced magnetic resonance imaging revealed sellar and pituitary stalk lesions, with iso- or hypodense signals on T1-weighted images. Transsphenoidal surgery was performed in three cases. It was challenging to diagnose hypophysitis due to the lack of any significant specific clinical signs. A transsphenoidal biopsy with fast-frozen pathology is able to diagnose hypophysitis. Glucocorticoid therapy may be a potential treatment for hypophysitis, as complete removal of pituitary masses may disable pituitary function.

Propofol (2,6-diisopropylphenol) is one of the most commonly used intravenous anesthetics and possesses a number of non-anesthetic effects, including antitumor function. The aim of the present study was to elucidate the antitumor molecular mechanism of propofol on A549 and H1299 cells. A549 and H1299 cells were treated in the presence or absence of different concentrations (0, 60 or 120 µmol) of propofol for different durations (0, 24, 48 or 72 h), and proliferation was detected by MTT and colony formation assays; the protein levels of optineurin (OPTN) ubiquitination, HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1 (HACE1), methyl-CpG binding domain protein 3 (MBD3) and Microtubule-associated protein 1A/1B-light chain 3 were detected by immunoblotting or quantitative (q)PCR; the methylation state of the HACE1 gene promoter was detected by bisulfite DNA sequencing; and binding of MBD3 on HACE1 gene promoter was detected by chromatin immunoprecipitation-qPCR. Propofol inhibited proliferation of A549 and H1299 cells and promoted HACE1-OPTN axis-mediated selective autophagy activity by increasing the protein expression levels of HACE1 via demethylating its promoter region. Furthermore, propofol promoted expression levels of MBD3 and binding to the -1,000 to -1 bp (transcription start site) region of HACE1 gene promoter. MBD3-knockdown experiments indicated that propofol inhibited proliferation of A549 cells in a MBD3-dependent manner. Thus, the findings of the present study provided a potential antitumor molecular mechanism mediated by propofol.

Lung cancer is amongst the most common types of cancer throughout the world. The overall 5-year survival rate is ~17%. A number of studies have demonstrated that the microbiome existing within the host may affect the level of inflammation, and consequently contribute to the carcinogenesis of certain types of cancer. To investigate the role of inflammation and the microbiome in the carcinogenesis of lung cancer, an intervention study involving mice, including a control group (C; n=5), a urethane-induced pulmonary adenocarcinoma group (U; n=5) and a prebiotics intervention group (P; n=5) was carried out. This pulmonary adenocarcinoma model was reviewed, and incidences of the disease were identified using histopathology. The levels of the inflammatory cytokines nuclear factor κB (NF-κB), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and IL-6 in the sera samples were measured using an ELISA technique. In addition, high-throughput sequencing of the 16S ribosomal RNA gene segment was used to analyze the species present in the microbiome of the lower airways and intestinal tracts of mice. The results demonstrated that groups P and U exhibited altered histopathology and the development of lung adenocarcinoma tumors, but no differences were observed between the groups. The level of inflammation, determined by measuring the levels of NF-κB, TNF-α, IL-1β and IL-6 inflammatory cytokines, was significantly lower in group P compared with group U (P

The aim of the present study was to examine the role of ABT-737, an inhibitor of B-cell lymphoma 2 (Bcl-2), in enhancing the effect of irradiation on uterine cervical cancer. Based on The Cancer Genomic Atlas (TCGA), Bcl-2 mRNA expression was associated with the Tumor-Node-Metastasis stage of cervical cancer. Therefore, it was hypothesized that Bcl-2 inhibition may decrease the progression of cervical cancer. ABT-737 was added to irradiation treatment to evaluate its effectiveness in inhibiting cancer cell progression. SiHa and CaSki cervical cancer cells were selected for in vitro assays. Patients with advanced stage III uterine cancer had slightly increased mRNA expression levels of Bcl-2 compared with patients with stage I cancer, although the difference was not significant. ABT-737 and radiation administration induced a synergistic cytotoxic effect based on the MTT assay and flow cytometry results, where an increase in apoptosis was observed. The apoptotic percentages were significantly increased in the cells treated with a combination of ABT-737 and irradiation. Loss of mitochondrial membrane potential and gain of reactive oxygen species (ROS) were detected by flow cytometry in CaSki and SiHa cells treated with ABT-737 and radiation. Additionally, the protein expression levels of the cleaved forms of poly ADP ribose polymerase and caspase-7 were increased following the combined treatment. In conclusion, ABT-737 and irradiation may induce apoptosis via loss of mitochondrial membrane potential and a ROS-dependent apoptotic pathway in CaSki and SiHa cells. The present study indicates that ABT-737 may be a potential irradiation adjuvant when treating cervical cancer.

The clinical efficacy of percutaneous vertebroplasty (PVP) and percutaneous kyphoplasty (PKP) in the treatment of osteoporotic vertebral compression fractures after bilateral resection of ovarian cancer was investigated. Eighty-six patients with osteoporotic vertebral compression fractures after bilateral resection of ovarian cancer admitted to the Second People's Hospital of Hefei from September, 2015 to August, 2016 were selected and randomly divided into control group (n=43) and observation group (n=43). The control group was treated with PVP, while the observation group received PKP. The operation time, fluoroscopy times, bone cement volume and leakage rate of patients in the two groups were recorded; the postoperative pain of patients was compared using Short-form McGill Pain Questionnaire; the changes in height of injured vertebra and Cobb angle of patients in two groups were compared; the efficacy of patients in the two groups was compared in accordance with Oswestry dysfunction index (ODI) and Japanese Orthopedic Association (JOA) low back pain scoring; and the quality of life was compared. The fluoroscopy times and bone cement leakage were significantly less in observation group than those in control group (P

The aim of the present study was to predict the prognostic value of 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) in the metastatic lymph nodes (mLNs) of patients with papillary thyroid carcinoma (PTC) with a negative iodine-131 (131I) whole-body scan (WBS). The present retrospective study included 32 patients with PTC undergoing standard surgery and radioiodine treatment. All patients received 18F-FDG PET/CT imaging prior to and following therapy. All mLNs were divided into an effective treatment group (group A) and ineffective treatment group (group B) based on the PET Response Criteria in Solid Tumors 1.0 guidelines. All the patients were followed up for ≥9 months. A significant difference was identified in the peak standardized uptake value (SULpeak) between group B (7.85±3.20) and group A (5.36±2.19). A cut-off value of 5.85 was used to distinguish ineffective treatment of lesions from mLNs receiving radioactive ablation based on receiver operating characteristic (ROC) curve analysis with an area under the ROC curve of 0.755. Patients with a high SULpeak (P=0.003) and extrathyroidal extension (P=0.030), confirmed by pathology, more frequently exhibited a poor prognosis. In conclusion, tracer uptake of 18F-FDG for cervical metastatic nodes was revealed as a predictor for the clinical outcome of patients with PTC treated with radioiodine therapy. The present results also indicated that high SULpeak and extrathyroidal extension are poor predictors for patients with mLNs receiving 131I therapy.

Oral tongue squamous cell carcinoma (OTSCC) is the most common type of oral cancer. Despite advances in knowledge regarding the genome-scale gene expression pattern of oral cancer, the molecular portrait of OTSCC biology has remained unclear over the last few decades. Furthermore, studies concerning OTSCC gene-expression profiles are limited or inconsistent owing to tissue heterogeneity in single-cohort studies. Consequently, the present study integrated the profile datasets of three cohorts in order to screen for differentially expressed genes (DEGs), and subsequently identified the potential candidate genes and pathways in OTSCC through gene enrichment analysis and protein-protein interaction (PPI) network construction. Using the selected Gene Expression Omnibus datasets GSE13601, GSE31056 and GSE78060, 206 DEGs (125 upregulated and 81 downregulated) were identified in OTSCC, principally associated with extracellular matrix (ECM) organization and the phosphoinositide 3-kinase/protein kinase B signaling pathway. Furthermore, 146/206 DEGs were filtered into the PPI network and 20 hub genes were sorted. Further results indicated that the two most significant modules filtered from the PPI network were associated with ECM organization and human papillomavirus infection, which are important factors affecting OTSCC pathology. Overall, a set of OTSCC-associated DEGs has been identified, including certain key candidate genes that may be of vital importance for diagnosis, therapy and prevention of this disease.

Lung cancer is amongst the most common types of cancer throughout the world. The overall 5-year survival rate is ~17%. A number of studies have demonstrated that the microbiome existing within the host may affect the level of inflammation, and consequently contribute to the carcinogenesis of certain types of cancer. To investigate the role of inflammation and the microbiome in the carcinogenesis of lung cancer, an intervention study involving mice, including a control group (C; n=5), a urethane-induced pulmonary adenocarcinoma group (U; n=5) and a prebiotics intervention group (P; n=5) was carried out. This pulmonary adenocarcinoma model was reviewed, and incidences of the disease were identified using histopathology. The levels of the inflammatory cytokines nuclear factor κB (NF-κB), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and IL-6 in the sera samples were measured using an ELISA technique. In addition, high-throughput sequencing of the 16S ribosomal RNA gene segment was used to analyze the species present in the microbiome of the lower airways and intestinal tracts of mice. The results demonstrated that groups P and U exhibited altered histopathology and the development of lung adenocarcinoma tumors, but no differences were observed between the groups. The level of inflammation, determined by measuring the levels of NF-κB, TNF-α, IL-1β and IL-6 inflammatory cytokines, was significantly lower in group P compared with group U (P0.05), and was significantly higher in group P compared with group C (P0.05). Overall, the microbiomes of the lower respiratory and intestinal tracts did not change markedly among the 3 groups, in terms of the size of colonies and Shannon diversity indices. However, at a family and operational taxonomic unit (OTU) level, certain microbiota were altered. For example, the abundance of the Clostridiales and Lachnospiraceae families was lower in the lung and intestinal tracts subsequent to urethane-induced treatment compared with in the control group (P0.05), and the level of abundance of the Clostridiales family increased to similar levels within the control group (P0.05), when prebiotics were administered. The levels of abundance of the S24-7, Bacteroidales and Firmicutes families were higher in the intestinal tract compared with the control group (P0.05), and following treatment with prebiotics, the levels of abundance of these families decreased to similar levels observed in the control group (P0.05). In conclusion, inflammation and the microbiome serve important roles in the carcinogenesis of lung cancer. Additionally, prebiotics may increase the efficacy of lung cancer treatment by modulating levels of inflammation and the composition of the microbiome. The associations between inflammation, the microbiome and lung cancer require attention.

The current study aimed to evaluate the expression and specific role of miR-26a-5p in the progression of bladder cancer (BC). Reverse transcription-quantitative polymerase chain reaction analysis was performed to evaluate the level of miR-26a-5p in BC cancer and healthy controls. The present data showed that plasma miR-26a-5p was significantly increased in BC patients. Furthermore, BC tissues exhibited greater levels of miR-26a-5p compared with adjacent non-neoplastic tissues-26a-5p. Compared with BC patients at Ta-T1 stage, the level of miR-26a-5p was significantly elevated in BC patients ≥T2. BC patients at G3 stage demonstrated a higher plasma miR-26a-5p level compared with those at G1/2 stage. Receiver operating characteristic (ROC) analysis indicated that miR-26a-5p could differentiate BC patients from controls. Additionally, Kaplan-Meier analysis demonstrated that plasma miR-26a-5p negatively correlated with survival of BC patients. Dual luciferase reporter assay indicated that miR-26a-5p significantly suppressed the relative luciferase activity of pmirGLO-PTEN-3′UTR compared with the control. In conclusion, the current study indicated novel data that the levels of plasma miR-26a-5p was significantly increased in BC patients. Furthermore, the present study suggested that determination of plasma miR-26a-5p level could help to distinguish BC patients from healthy controls via targeting PTEN.

Oridonin, the main active constituent of Rabdosia rubescens, is known to exert antitumor activity via the induction of apoptosis in numerous types of human cancer cells. However, the underlying regulatory mechanisms of mitochondrial ROS in oridonin-induced HepG2 apoptosis remain largely unknown, due to limitations of subcellular imaging resolution. Previously, it has been suggested that mitochondria serve a potential role in sensing and signaling cellular redox changes in vital biological processes such as cell death and the abiotic stress response, based on studies involving the mitochondrial-targeted redox-sensitive green fluorescent protein (GFP). To address this, a mitochondrial-targeted Grx1-roGFP2 (mtGrx1-roGFP2) biosensor was implemented to monitor real-time mitochondrial redox changes of HepG2 cells in response to either H2O2/DTT or oridonin/SS31 treatment. It was determined that oridonin caused a perturbation in mitochondrial redox status, which in turn contributed to oridonin-induced apoptosis. Furthermore, a novel mechanism underlying the regulation of mitochondrial redox changes in oridonin-induced HepG2 apoptosis, presumably dependent on PARP cleavage, was proposed. In conclusion, the present study provides evidence in support of mitochondrial redox changes as a potential mediator in the apoptotic activities of oridonin in HepG2 cells, which provides insight into the molecular mechanisms by which mitochondrial redox signaling regulates oridonin-induced apoptosis in cancer therapy, and the development of mitochondria-specific oridonin as a promising novel anticancer therapeutic strategy.

The aim of the present study was to investigate whether oridonin is able to increase the effects of lentinan (LNT) in HepG2 human hepatoblastoma cells by MTT, flow cytometry, reverse transcription-quantitative polymerase chain reaction and western blot analysis. The in vitro results demonstrated that 20 µg/ml of oridonin was a nontoxic concentration for L02 normal liver cells and HepG2 liver cancer cells. Furthermore, treatment with 0–200 µg/ml LNT was only able to decrease the viability of HepG2 liver cancer cells. The growth inhibitory rate of the LNT-L (100 µg/ml) treatment group was 20.7% and the rate of the LNT-H (200 µg/ml) treatment group was 54.8%. Notably, the growth inhibitory rate of the oridonin + LNT-H group was 84.3%. The highest percentage of apoptotic cells was observed in the oridonin + LNT-H group (20 µg/ml oridonin and 200 µg/ml LNT). The percentage of apoptotic cells in the oridonin + LNT-H group was significantly different from the percentage of apoptotic cells in the LNT-H (26.1%) and the LNT-L (16.8%) groups. Treatment with LNT produced an increase in caspase-3, caspase-9, Bcl-2-like protein 4, p53, p21, nuclear factor κB inhibitor-α mRNA and protein expression and a decrease in B-cell lymphoma 2 and nuclear factor-κB expression in HepG2 cells compared with untreated control cells. Treatment with a combination of oridonin and LNT-H induced a further increase in expression with the biggest differences in expression observed between the oridonin + LNT-H group and control. It was observed that treatment with oridonin was able to increase the anticancer effects of LNT in HepG2 cells. Therefore, oridonin may be used to sensitize cells to LNT.

The aim of the present study was to investigate the effect of the combination of interventional adenovirus-p53 (Ad-p53) introduction and ultrasonic irradiation (CIAIUI) treatment for liver cancer, including evaluating the Ad-p53 transfection efficiency and the impact of the p53 gene on vascular endothelial growth factor (VEGF) and matrix metalloprotein 2 (MMP2) protein expression levels. Ad-p53 was arterially infused into the hepatic carcinoma via the interventional introduction of the hepatic tumor-bearing artery (IIHTBA) or the CIAIUI. Serum VEGF levels were determined by performing an enzyme-linked immunosorbent assay; immunohistochemical analysis was used to identify the expression levels of intratumoral p53, MMP2 and VEGF; and western blot analysis was used to determine the impact of different Ad-p53 administration methods on the expression of wild-type p53. The wild-type p53 expression level was significantly higher in the p53-treated group compared with the control group, and the p53 expression level in the CIAIUI group was significantly higher compared with the non-irradiation group. The CIAIUI could significantly reduce the serum VEGF levels. The two delivery methods caused a reduction in the intratumoral VEGF and MMP2 expression levels, and the effects of CIAIUI were most obvious. Ad-p53 infusion via IIHTBA promoted the protein expression levels of p53, however, it inhibited the protein expression levels of MMP2 and VEGF, indirectly indicating that the gene may inhibit the growth of liver cancer. Therefore, CIAIUI therapy exhibited an overall improved therapeutic effect compared with the more simple IIHTBA therapy.

Cancer stem cells are enriched in triple-negative breast cancer (TNBC) tumor tissues, which present strong capacities of proliferation and tumorigenicity. The present study detected the distribution of cancer stem cell markers cluster of differentiation (CD)44/CD24 and analyzed the clinical outcomes of different CD44/CD24 phenotypes in patients with TNBC. Multivariate Cox regression analyses were performed with regard to the prognostic value of cancer stem cell markers CD44/CD24, aldehyde dehydrogenase 1 and other baseline clinical characteristics, including tumor size, lymph node involved, adjuvant chemotherapy, Ki-67, breast cancer susceptibility gene 1, cellular tumor antigen p53, vimentin and basal-like status. The multivariate analyses showed that three of these factors, CD44/CD24 phenotype, basal-like status and number of lymph nodes involved, had an impact on overall survival. Furthermore, patients with CD44+/CD24− phenotype, basal-like tumors and ≥4 lymph nodes involved had a significantly worse prognosis. The expression of CD44 and CD24 was detected by double-staining immunohistochemistry, which can locate cancer stem cells individually. Overall, the present results indicated that CD44/CD24 status evaluated by double-staining immunohistochemistry constitutes an independent prognostic factor for TNBC.

The increased expression of cluster of differentiation (CD)47 has been identified in a number of different tumor types and is recognized as an adverse prognostic factor that indicates an increased risk of mortality in patients. The binding of CD47 to signal regulatory protein α (SIRPα) inhibits the macrophage phagocytosis of tumor cells by triggering an inhibitory 'do not eat me' signal. This is one of the mechanisms used by tumor cells to evade immune surveillance. In the present study, CD47 levels and macrophage infiltration were assessed in patients with esophageal squamous cell cancer (ESCC). CD47-overexpressing ESCC cell lines were selected and human M2 macrophage phagocytic activity was measured. The results revealed that CD47 is highly expressed and macrophages are markedly infiltrated in cancerous tissue compared with non-cancerous tissue. High CD47 expression was detected in ESCC cell lines and the results of a phagocytosis assay indicated that human M2 macrophages phagocytized tumor cells in a dose-dependent manner following the blocking of CD47-SIRPα signaling by anti-CD47 antibodies. The results of the present study therefore support the use of anti-CD47 immunotherapy to treat patients with ESCC.

The RAS/RAF and PI3K/PTEN signaling pathways play central roles in hepatocarcinogenesis. KRAS, NRAS, HRAS, BRAF, PIK3CA, PIK3R1 and PTEN are key cancer-related genes in the RAS/RAF and PI3K/PTEN signaling pathways. Genetic alterations in these genes often lead to the dysregulation of the two cascades. Little is known regarding the frequency of hotspot mutations in these critical components among Chinese patients with hepatocellular carcinoma (HCC). In the current study, 57 somatic hotspot mutations in 36 HCCs samples collected from Chinese patients using direct DNA sequencing method were examined. Two cases of KRAS somatic mutations (KRAS codon 61; Gln to His) were identified among 36 HCCs (5.6%). However, no mutations were found in the NRAS, HRAS, BRAF, PIK3CA, PIK3R1 and PTEN genes. These findings indicated that point mutations in the KRAS gene, but not mutations in NRAS, HRAS, BRAF, PIK3CA, PIK3R1 and PTEN genes, at a somatic level contribute to the abnormal activation of the RAS/RAF and PI3K/PTEN pathways in HCC.

Ovarian cancer is the most fatal gynecological cancer, with a 5-year survival rate of only 30%. Lysophosphatidic acid (LPA), which possesses growth factor-like functions, is a major regulatory factor in the peritoneal metastasis of ovarian cancer. LPA stimulates the expression of numerous genes that are associated with angiogenesis and metastasis. Ovarian epithelial carcinoma specifically expresses chemotactic factor C-X-C motif chemokine ligand 12 (CXCL12) and its receptor, CXC receptor 4 (CXCR4). The CXCL12-CXCR4 axis directly contributes to ovarian cancer cell proliferation, migration and invasion. The present study investigated the regulation of LPA on the CXCL12-CXCR4 axis and the effect of the LPA-mediated CXCL12-CXCR4 axis on the tumor proliferation, migration and invasion of ovarian cancer cell lines. The CXCR4 proteins expressed in the cell membrane and the cytoplasm of ovarian cancer cells, CAOV3 and SKOV3, were detected by immunocytochemistry. The expression of CXCR4 and CXCL12 was increased in the ovarian cancer cells in a dose- and time-dependent manner when treated with LPA compared with the control groups (P

The abscopal effect has previously been described in various tumors and is associated with radiation therapy and hyperthermia, with possible underlying mechanisms explaining each observed case. In the present study, we aimed to investigate the antitumor effects of magnet-mediated hyperthermia on Walker-256 carcinosarcomas in rats at two different temperature ranges (42–46°C and 50–55°C). We also aimed to identify whether a higher therapeutic temperature of magnetic-mediated hyperthermia improves the abscopal antitumor effects, where localised irradiation of the tumor causes not only the irradiated tumor to shrink, but also tumors located far from the area of irradiation. Following induction of carcinosarcoma in both sides of the body, magnet-mediated hyperthermia was applied to one side only, leaving the other side as a control. The changes in tumor growth were observed. Our results demonstrated that magnet-mediated hyperthermia at a higher temperature inhibited the growth of carcinosarcoma at the site of treatment. Furthermore, the growth of the carcinosarcoma on the untreated side was also inhibited. The expression levels of proliferating cell nuclear antigen were decreased in the hyperthermia group, which was more significant in the higher temperature test group. Flow cytometric analysis showed an increased number of CD4- and CD8-positive T cells, and enzyme-linked immunosorbent assay showed increased levels of interferon-γ and interleukin-2 in the higher temperature group. These results suggested that magnet-mediated hyperthermia at a higher temperature (50–55°C) can improve the abscopal antitumor effects and stimulate a greater endogenous immune response in carcinosarcoma-bearing rats.

Acute promyelocytic leukemia (APL) is characterized by the presence of the promyelocytic leukemia (PML)-retinoic acid receptor-α (RAR-α) fusion protein. PML-RARα can be cleaved by neutrophil elastase (NE) in several positions in cells in the promyelocytic stage, nuclear location signal (NLS)-negative PML and NLS-RARα may be the products of PML-RARα by NE. The function of NLS-RARα may be affected by the addition of NLS, which would alter its localization in cells, as the role of NLS is to identify proteins for transport to the nucleus. Preliminary experiments demonstrated that the overexpression of NLS-RARα in HL-60 cells could promote cellular proliferation and inhibit cellular differentiation. Following treatment with all-trans retinoic acid (ATRA), the degree of cellular differentiation was enhanced. In the present study, the localization of NLS-RARα was identified and its activity as a novel transcriptional factor was assessed, which may be critical in the development of APL. The location of NLS-RARα was detected in the nucleus and cytoplasm by indirect immunofluorescence and western blot analysis, with expression in the nucleus revealed to be increased compared with that in the cytoplasm. Next, native-PAGE was performed and NLS-RARα and RXRα were revealed to form heterodimers in the nucleus. In addition, co-immunoprecipitation revealed an interaction between NLS-RARα and retinoid X receptor-α (RXRα). An electrophoresis mobility shift assay (EMSA) indicated that NLS-RARα could bind retinoic acid response elements (RAREs) in the presence of ATRA. Indeed, NLS-RARα could bind RAREs just as WTRARα could, including the RAREs direct repeat-2 (DR-2) and DR-5. In addition, results from a luciferase reporter gene assay demonstrated that NLS-RARα could mediate the activity of RAREs that it bound. Together, these results indicated that NLS-RARα may be a novel transcription factor that contributes to leukemogenesis by competitively binding RAREs as heterodimers with RXRα, just as PML-RARα does, thus repressing the gene transcription essential for myeloid differentiation. These findings indicate the potential role of NLS-RARα targeted therapy in APL.

The epithelial-mesenchymal transition plays a crucial role in the progression of pancreatic cancer. The aim of this study was to examine the possible association between the epithelial-mesenchymal transition and cancer stem-like cells in pancreatic cancer. We used transforming growth factor β to induce an epithelial-mesenchymal transition. The proportion of pancreatic cancer stem-like cells was measured and sorted by flow cytometry. The expression of markers was measured by quantitative PCR and Western blot analysis. Cell cycle distribution was assessed by flow cytometry. We evaluated the migration and invasion activity by Transwell tests. The proportion of pancreatic cancer stem-like cells was significantly increased following transforming growth factor β treatment. Cells were sorted in culture, the cancer stem-like cells exhibited a higher degree of epithelial-mesenchymal transition and demonstrated upregulation of vimentin, a mesenchymal phenotypic marker, compared to the CD44(-)CD24(-) cells. Pancreatic cancer stem-like cells exhibited greater invasion and migration activity in vitro compared to the CD44(-)CD24(-) cells. These results suggested a direct link between epithelial-mesenchymal transition and cancer stem-like cells in pancreatic cancer.

Primary malignant melanoma (MM) of the uterine cervix is a rare neoplasm and the overall prognosis of patients with this disease is poor. Immunohistochemical methods and exclusion of other primary melanoma sites are used to confirm the diagnosis. In the present study, the case of a 65-year-old female patient with an MM of the uterine cervix is reported. Diagnosis was confirmed by immunohistochemical methods using human melanoma black 45 antibody and S-100 protein. The tumor was identified as stage IB1 using the International Federation of Gynecology and Obstetrics classification. Chest X-ray and abdominopelvic computed tomography results were normal. The patient subsequently underwent a radical hysterectomy with bilateral salpingo-oophorectomy and pelvic lymphadenectomy. Following combined radical surgery and chemotherapy, complete remission of the tumor was achieved. The patient has since been well for 30 months without recurrence subsequent to the surgery.

Dermatofibrosarcoma protuberans (DFSP) is a rare, metastasizing tumor of the deep dermis and subcutaneous tissue. While it frequently occurs in the trunk and extremities, breast involvement has rarely been reported. In the present case, imaging and pathological technologies were used to detect DFSP of the breast. Surgical excision with wide margins (>3 cm) and pathology revealed spindle cells arranged in storiform patterns and short fascicles which were crucially CD34-positive, enabling a definitive diagnosis prior to surgery.

A component purified from Strongylocentrotus nudus eggs on a diethylaminoethyl cellulose-52 chromatography column and eluted using a NaCl solution gradient (SEP-S), is a homogeneous polysaccharide of α-D-glucan with a reduced molecular weight of 9.33×105 Da, compared with that of S. nudus egg polysaccharide (SEP). In an in vivo antitumor assay of histocompatibility-22 hepatocellular carcinoma in tumor-bearing mice, the inhibitory rates at SEP-S doses of 5, 10 and 20 mg/kg/day were 38.8, 50.7 and 70.3%, respectively. In addition, the spleen and thymus indices and the percentages of cluster of differentiation (CD) 4+ and CD8+ T cells were significantly increased, and the activity of cytotoxic T lymphocytes was notably enhanced, suggesting that the anti-hepatocellular carcinoma activity is mediated by boosting the immune system. In vitro experiments also demonstrated that splenocyte proliferation induced by SEP-S was inhibited by the toll-like receptor (TLR) 2 and TLR4 monoclonal antibodies. These data indicate that SEP-S is a polysaccharide component possessing high anti-hepatocellular carcinoma activity and may be a potential immunotherapy candidate for the treatment of liver cancer.

Pancreatic hamartoma is an extremely rare, non-neoplastic, mass-forming lesion that may be mistaken for malignancy, and the pre-operative diagnosis is particularly challenging. The published literature contains only 23 cases of pancreatic hamartoma. The majority of the cases reported patients with a single benign tumor-like disease that received a pancreatectomy. Immunohistochemical findings confirmed the diagnosis following surgery. The current study reports the case of a 53-year-old female who presented to the Department of Abdominal Surgery, Chinese Academy of Medical Sciences, Cancer Hospital (Beijing, China), due to abdominal pain. Abdominal magnetic resonance imaging revealed a 22×14-mm mass in the head of the pancreas. The patient was pre-operatively diagnosed with a pancreatic space-occupying lesion, and subsequently underwent a pancreaticoduodenectomy. The post-operative course was uneventful. Histological examination of the resected lesion resulted in a diagnosis of pancreatic hamartoma. There were no signs of recurrence at 55 months post-surgery.

Primary sarcoma of the aorta is extremely rare and accounts for

Synchronous multiple primary cancers are relatively uncommon and synchronous multiple cancers in coexistence with dermatomyositis (DM) are extremely rare. In the present study, we report a case of a 64-year-old male with nasopharyngeal undifferentiated non-keratinizing carcinoma and cardia adenocarcinoma which were diagnosed synchronously. In addition, suspected DM was diagnosed during the course of chemotherapy. The symptoms of DM were exaggerated even when methylprednisolone while administered. The patient succumbed to nutritional deterioration four months following his initial admission. In the present study, the etiologies of multiple primary cancers are discussed and a brief review of the literature on the correlation between malignance and DM was conducted.

In recent years, asparaginase-based chemotherapy regimens have produced excellent short-term efficacy in patients with extranodal natural killer/T-cell lymphoma (ENKTL). However, few long-term outcomes have been reported to date. A phase II clinical trial evaluating the efficacy and safety of a combination of gemcitabine, oxaliplatin and asparaginase (GELOX), followed by radiotherapy (RT) in the treatment of localized ENKTL, was reported by this group in 2012. By the time of the present analysis, detailed information had been collected for all 27 patients in the phase II trial, over an extended follow-up period. The median follow-up time was 63.15 months. The 5-year overall survival and progression-free survival were 85.0 and 74.0%, respectively. Recurrence within the RT field was observed in three patients, and the planning target-volume control rate at 5 years was 88.9%. One patient with confirmed lung invasion who did not respond to autologus stem cell transplantation (ASCT) was successfully treated by salvage therapy with lenalidomide monotherapy, and the EBV DNA load in this individual reflected disease progression and treatment response. No clinically significant late toxicities were identified during follow-up visits. In conclusion, this updated analysis confirmed the long-term benefit of the GELOX regimen followed by RT, and demonstrated a good safety profile for this treatment. This strategy may be one of the most suitable options for the treatment of early stage ENKTL.

Metastasis-associated in colon cancer 1 (MACC1) is a newly identified gene that has been shown to promote tumor cell invasion and metastasis. The present study investigated the effect of MACC1 downregulation on the biological characteristics of the ovarian cancer OVCAR3 cell line. In this study, MACC1 expression was blocked using the RNA interference technique. The downregulation of MACC1 mRNA and protein expression was confirmed using quantitative polymerase chain reaction and western blot analysis. The proliferative activity and adhesion rate of the cells were detected using cell counting kit-8 and a cell adhesion assay, while cell invasion was determined using a Matrigel invasion assay and migration capacity was observed using migration and wound-healing assays. A tube formation assay was also used to examine the angiogenic capacity of cells, and a luciferase assay was performed to assess whether MACC1 binds to the c-MET gene. The MACC1 mRNA and protein expression levels were significantly downregulated using sequence-specific small interfering RNA (siRNA). The inhibition of MACC1 expression markedly decreased the invasive, metastatic and angiogenic capacities of the cells, but only slightly inhibited growth and adhesion. In addition, a putative MACC1-binding site was identified in the 3′-untranslated region of c-MET. MACC1-siRNA was also found to significantly reduce the expression of the c-MET protein and a luciferase reporter assay confirmed that c-MET was the target gene of MACC1. These results demonstrated that the attenuation of MACC1 suppresses cell invasion and migration and that MACC1 may regulate cell metastasis through targeting the expression of c-MET. Inhibition of the function of MACC1 may represent a new strategy for treating ovarian cancer.