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The present study aimed to assess the correlation of C-X-C motif chemokine ligand (CXCL)1, CXCL2, CXCL8, CXCL13 and CXCL14 with clinicopathological features and survival profile in patients with colorectal cancer (CRC). Patients with primary CRC (n=232) were retrospectively reviewed, with their tumor tissue specimens acquired from the Department of Pathology (The First Hospital of Jilin University, Changchun, China), their demographic data and preoperative tumor features collected from the hospital database, and their survival data obtained from the follow-up documents. Tumor CXCL expression was detected by immunohistochemistry (IHC). Based on the total IHC score, the expression of CXCL1, CXCL2, CXCL8, CXCL13 and CXCL14 was categorized as low expression (IHC score ≤3) and high expression (IHC score3). CXCL1 (51.3% high and 48.7% low), CXCL2 (59.9% high and 40.1% low), CXCL8 (44.4% high and 55.6% low), CXCL13 (40.9% high and 59.1% low) and CXCL14 (31.0% high and 69.0% low) were expressed in CRC tumor tissues, and their expression levels were correlated with each other, except between CXCL8 and CXCL14, and between CXCL13 and CXCL14. CXCL1 was associated with a larger tumor size, and an advanced T stage, N stage and Tumor-Node-Metastasis (TNM) stage. CXCL2 was associated with an advanced N stage and TNM stage, and CXCL8 was associated with a greater T stage and TNM stage. CXCL13 was associated with a greater T stage, N stage and TNM stage, while CXCL14 was not associated with any clinical characteristics. As for survival, CXCL1, CXCL2, CXCL8 and CXCL13, but not CXCL14, were associated with poor overall survival (OS) rate, and further multivariate Cox's regression model analysis revealed that CXCL1 independently predicted unfavorable OS in patients with CRC. Overall, CXCL1, CXCL2, CXCL8 and CXCL13 have good potential as an indicator for tumor features and survival in patients with CRC.

Cisplatin resistance has been a major factor limiting its clinical use as a chemotherapy drug. The present study aimed to investigate whether SET and MYND domain-containing protein 3 (SMYD3), a histone methyltransferase closely associated with tumors can affect the sensitivity of tumors to cisplatin chemotherapy. Real time-qPCR, western blotting, the luciferase reporter, MTT and clonogenic assays were performed to detect the effects of SMYD3 on the chemotherapy capacity of cisplatin. In the present study, SMYD3 exhibited different expression patterns in MCF-7 and T47D breast cancer cells. In addition, this differential expression was associated with tumor cell resistance to cisplatin. Furthermore, SMYD3 knockdown following small interfering RNA transfection increased cisplatin sensitivity, whereas SMYD3 overexpression decreased cisplatin sensitivity. In addition, SMYD3 knockdown synergistically enhanced cisplatin-induced cell apoptosis. SMYD3 expression was downregulated during cisplatin treatment. In addition, transcriptional regulatory activities of SMYD3 3'-untranslated region were also downregulated. These results suggested that SMYD3 may affect cell sensitivity to cisplatin and participate in the development of cisplatin resistance, which is a process that may involve microRNA-124-mediated regulation.

Erastin is a small molecular compound that induces ferroptosis by binding to voltage-dependent anion-selective channel protein (VDAC)2, VDAC3 and solute carrier family 7 member 5 inhibiting the cystine/glutamate antiporter. However, to the best of our knowledge, the mechanism of erastin-induced breast cancer cell death remains unclear. In present study aimed to explore the underlying mechanisms of the antitumor effects of erastin on breast cancer cells. Cellular viability was assessed using an MTT assay, a lactate dehydrogenase cytotoxicity assay kit was used to determine the cell death rate, the intracellular Fe2+ levels were determined using an iron colorimetric assay kit and western blotting was used to estimate the changes of autophagy-associated proteins levels. The present study demonstrated that erastin inhibited the viability of breast cancer cells and induced breast cancer cell death in a dose-dependent manner. Additionally, autophagy was activated by erastin, as demonstrated by upregulated expression levels of autophagy-associated proteins in breast cancer cells. Bafilomycin A1, 3-methyladenine and knockdown of autophagy related (ATG)5 with small interfering RNA prevented erastin-induced breast cancer cell death and inhibited the erastin-induced changes in the expression levels of the autophagy-associated proteins beclin1, ATG5, ATG12, microtubule-associated proteins 1A/1B light chain 3B (LC3B) and P62. Furthermore, erastin-induced breast cancer cell death was inhibited by an iron chelator, deferoxamine, which inhibited the increases of erastin-induced iron levels and inhibited the erastin-induced changes in the expression levels of the autophagy-related proteins beclin1, ATG5, ATG12, LC3B and P62. In summary, erastin triggered autophagic death in breast cancer cells by increasing intracellular iron levels.

Esophageal cancer (EC) is the eighth most common type of cancer worldwide and ranks sixth among the causes of cancer-related mortality. Due to the high mortality rate and poor treatment efficacy for EC, millions of individuals succumb to this disease; thus, the identification of novel treatment targets is of utmost importance and urgency. In recent years, there have been advances if therapies targeting cell cycle regulators. p21 is a type of cell cycle regulator that plays a dual role in tumor cells, as it can not only regulate the cell cycle, induce apoptosis and inhibit cell proliferation, but can also protect cells from apoptosis. It has been found that p21 often exerts a tumor-suppressive effect on EC, which provides a basis for its use as a treatment target for EC. Therefore, the aim of the present study was to review the function of p21 and its potential value as a therapeutic target for EC.

Clear cell renal cell carcinoma (ccRCC) is one of the most common tumor types of the urinary system. Bioinformatics tools have been used to identify new biomarkers of ccRCC and to explore the mechanisms underlying development and progression of ccRCC. The present study analyzed the differentially expressed genes (DEGs) associated with RCC using data obtained from Gene Expression Omnibus datasets and GEO2R software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of these DEGs was performed and analyzed using the Database for Annotation, Visualization and Integrated Discovery. A protein-protein interaction (PPI) network was constructed using the Search Tool for the Retrieval of Interacting Genes to identify the hub genes, defined as the genes with the highest degree of interrelation. Subsequently, differential expression and survival analyses of hub genes was performed using The Cancer Genome Atlas database and Gene Expression Profiling Interactive Analysis (GEPIA) online tool. Using GEO2R, 1,650 DEGs were identified, including 743 upregulated and 907 downregulated genes. GO and KEGG pathway analyses indicated that the upregulated DEGs were primarily involved in blood vessel and vasculature development, whereas downregulated DEGs were primarily involved in organic acid metabolic processes and carboxylic acid metabolic processes. Subsequently, important modules were identified in the PPI network using Cytoscape's Molecular Complex Detection. The 15 most connected hub genes were identified among DEGs, including glycine decarboxylase (GLDC), enolase 2 (ENO2) and topoisomerase II alpha. GEPIA revealed the association between expression levels of hub genes and survival. Specifically, GLDC and ENO2 were associated with the prognosis of patients with RCC and thus, the effects of GLDC and ENO2 involvement in renal cancer were investigated in vitro. GLDC and ENO2 affected the proliferation and apoptosis of renal cancer cells. These hub genes may reveal a new mechanism underlying development or progression of RCC and identify new markers for its diagnosis and prognosis.

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer in the world, yet current treatment options are associated with limited success. The aim of the present study was to investigate the expression of ferritin in HNSCC and clarify whether it may serve as a biomarker for predicting HNSCC metastasis. The chemiluminescent immunoassay method was used to investigate the differences in the serum ferritin (SF) levels between patients with and without tumors, and between HNSCC with and without lymph node metastasis. The iron content and expression levels of ferritin were detected to verify the differences between tumor and normal tissues, and between HNSCC without and with lymph node metastasis. Data from the Gene Expression Omnibus (GEO) dataset was used to support the aforementioned results. No statistically significant difference in the SF level was observed between patients with and without tumors. Iron content and expression levels of ferritin heavy chain (FTH) and ferritin light chain (FTL) were higher in tumor tissues compared with normal tissues. The iron content and expression levels of SF, FTH and FTL were increased in HNSCC with metastasis compared with HNSCC without metastasis. The GEO dataset further verified the results and reported that the expression level of FTH was correlated with the prognosis of patients with HNSCC. Ferritin may not be a biomarker for the early diagnosis of HNSCC. However, an association exists between the expression level of ferritin and HNSCC cervical metastasis. SF may be a potential biomarker for predicting cervical lymph node metastasis in patients with HNSCC.

Sarcomas arise from primitive mesenchymal cells, which are classified, into two main groups: Bone and soft tissue sarcomas. We have searched all-important electronic databases including Google scholar and PubMed for the collection of latest literature pertaining to pediatric sarcomas. Latest literature confirmed that these tumors are relatively rare and represent only 1% of all malignancies but they have higher incidence in children. Pediatric sarcomas comprise about 13% of all pediatric malignancies and are ranked third in childhood cancers. The highest incidence rates are reported among rhabdomyosarcoma, osteosarcoma and Ewing's sarcomas in children. All of these neoplasms often display highly aggressive behavior with tendency to form metastases. Important globally used management avenues include surgery with systemic chemotherapy and have success rate of 70% at 5-years. Furthermore, in the cases of advanced stages, the prognosis is poor, chances of treatment failure and recurrence are quite high. Utilization of cancer stem cells is the latest approach with great potential in management of above pathological state. The present review article discuss all-important aspects of commonly found pediatric sarcomas throughout the world.

Angiosarcoma is a rare soft tissue sarcoma, and the data about its clinicopathological features and prognostic factors are limited. The purpose of the present study was to report a large series of angiosarcoma at a single institution. Clinical data from 200 cases of angiosarcoma from the Shanghai Cancer Center (Shanghai, China) between March 2006 and March 2014 were retrospectively analyzed. The study population included 97 males and 103 females with ages between 4 and 91 years (median, 53 years). According to the tumor location, 200 cases were divided into 4 groups: i) Tumors involving the head and neck; ii) breast; iii) viscera (including internal organs and bone); and iv) soft tissue (including trunk and extremities). Of the 113 patients with follow-up data, 46 patients succumbed to the disease with a median interval of 10 months. Tumor recurrence/metastasis was identified in 66 patients with a median interval of 4 months. The disease-free survival (DFS) rate at 5-years was 19.3% and the overall survival (OS) rate at 5-years was 40.8%. Site of tumor origin, size (≥5 cm) and histological differentiation influenced DFS (P=0.032, 0.038 and

The cell cycle is a dynamic process with multiple phases regulating cell growth. The proper regulation is essential for avoiding errors and activation of cell death. Tumour suppressor proteins, including tuberin, are crucial in coordinating adequate cell growth and properly timed cell division. So, the present review article is focused on the latest aspects of the tuberin in the process of carcinogenesis. The PubMed was the main database used for the collection of latest data relating to multiple aspects of tuberin especially in context of cancer. Most of the recent studies revealed that mutation, truncation, and deregulation of the tuberin protein could definitely lead to cancer. Recent studies are also devoted to explore implications towards better understanding the progression of disease involving mis-regulated tuberin.

MicroRNAs (miRNAs) are short non-coding RNAs that regulate the expression of protein-coding genes by partially binding to specific target sites of mRNAs. miRNAs perform important functions in complicated cellular biological processes and their abnormal expression is involved in various disorders, including cancer. Among the miRNAs, differential expression of miR-139-5p serves a significant role in tumorigenesis, metastasis and recurrence, thus suggesting that it may potentially be used as a promising biomarker for cancer diagnosis, prognosis and therapy. miR-139-5p is expected to serve as a biomarker to eventually be implemented in a clinical setting. In the present review, we focus on the importance of miR-139-5p in cancer, summarize the association between miR-139-5p expression level and diagnosis and prognosis, and discuss the potential therapeutic implications for the future.

SET and MYND domain containing 3 (SMYD3) is a histone methyltransferase (HMT) and transcription factor, which serves important roles in carcinogenesis. Numerous downstream target genes of SMYD3 have been identified in previous studies. However, the downstream microRNA (miRNA) s regulated by SMYD3 are yet to be elucidated. In the present study, the results of miRNA microarray demonstrated that 30 miRNA expression profiles were upregulated, whilst 24 miRNAs were downregulated by >2.0-fold in the SMYD3-overexpressed MCF-7 breast cancer cells. The HMT activity was demonstrated to be essential for SMYD3-mediated transactivation of miR-200c-3p and the overexpression of miR-200c-3p inhibited the transactivation effects of SMYD3 on myocardin-related transcription factor-A-dependent migration-associated genes. To our best knowledge, the current study is the first to report on the transcriptional regulation of SMYD3 on miRNAs, and miR-200c may be a downstream negative regulator of the SMYD3-mediated pathway in the migration of breast cancer cells. These results may provide a novel theoretical basis to understand the mechanisms underlying the initiation, progression, diagnosis, prevention and therapy of breast cancer.

Emerging evidence has suggested that pancreatic adenocarcinoma is sustained by pancreatic cancer stem cells. The present study aimed to investigate the expression patterns of the pancreatic cancer stem cell surface markers cluster of differentiation CD44 and CD24 in a pancreatic adenocarcinoma cell line, and to investigate the possible mechanisms for their radiation resistance. Flow cytometry was used to analyze the expression patterns of CD44 and CD24 in the pancreatic adenocarcinoma PANC-1 cell line. In addition, a multi-target click model was used to fit cell survival curves and determine the sensitizer enhancement ratio. The apoptosis and cycle distribution of the four cell subsets was determined using flow cytometry, and the level of reactive oxygen species (ROS) was determined using the 2',7'-dichlorofluorescin diacetate probe. The present results identified that the ratios of CD44+ and CD24+ in the sorted PANC-1 cell line were 92.0 and 4.7%, respectively. Prior to radiation, no statistically significant differences were observed among the four groups. Following treatment with 6 MV of X-rays, the rate of apoptosis was decreased in the CD44+CD24+ group compared with other subsets. The percentage of G0/G1 cells was highest in the CD44+CD24+ group compared with the three other groups, which exhibited increased radiosensitivity. In addition, the level of ROS in the CD44+CD24+ group was reduced compared with the other groups. In summary, the results of the present study indicated that CD44+CD24+ exhibited stem cell properties. The lower level of ROS and apoptosis in CD44+CD24+ cells may contribute to their resistance to radiation in pancreatic adenocarcinoma.

Normal adult mammary stem cells (AMSCs) are promising sources for breast reconstruction, particularly following the resection of breast tumors. However, carcinogenic events can potentially convert normal AMSCs to cancer stem cells, posing a safety concern for the use of AMSCs for clinical tissue regeneration. In the present study, AMSCs and autologous primary breast cancer cells were isolated and compared for their ability to differentiate, their gene expression profile, and their potential to form tumors in vivo. AMSCs were isolated from normal tissue surrounding primary breast tumors by immunomagnetic sorting. The pluripotency of these cells was investigated by differentiation analysis, and gene expression profiles were compared with microarrays. Differentially expressed candidate genes were confirmed by reverse transcription-polymerase chain reaction and western blot analyses. The in vivo tumorigenicity of these cells, compared with low-malignancy MCF-7 cells, was also investigated by xenograft tumor formation analysis. The results revealed that AMSCs isolated from normal tissues surrounding primary breast tumors were positive for the stem cell markers epithelial-specific antigen and keratin-19. When stimulated with basic fibroblast growth factor, a differentiation agent, these AMSCs formed lobuloalveolar structures with myoepithelia that were positive for common acute lymphoblastic leukemia antigen. The gene expression profiles revealed that, compared with cancer cells, AMSCs expressed low levels of oncogenes, including MYC, RAS and ErbB receptor tyrosine kinase 2, and high levels of tumor suppressor genes, including RB transcriptional corepressor 1, phosphatase and tensin homolog, and cyclin-dependent kinase inhibitor 2A. When injected into nude non-obese diabetic/severe combined immunodeficiency-type mice, the AMSCs did not form tumors, and regular mammary ductal structures were generated. The AMSCs isolated from normal tissue adjacent to primary breast tumors had the normal phenotype of mammary stem cells, and therefore may be promising candidates for mammary reconstruction subsequent to breast tumor resection.

The present study aimed to identify differentially expressed inflammatory factors observed in Wilms tumors (WT), and to investigate the association of these factors with clinical stage, pathological type, lymph node metastasis and vascular involvement of WT. Surface-enhanced laser desorption/ionization-time of flight mass spectrometry was performed to screen differentially expressed proteins among WT and normal tissue pairs. Upregulated proteins in WT were separated and purified by solid phase extraction and Tricine SDS-PAGE, respectively. Following in-gel digestion, the peptide mixture was subjected to liquid chromatography mass spectrometry to identify proteins on the basis of their amino acid sequences. Immunohistochemistry was used to confirm the expression of differentially expressed inflammatory proteins. Of the proteins that were upregulated in WT, two proteins with mass/charge (m/z) ratio of 12,138 and 13,462 were identified as macrophage migration inhibitory factor (MIF) and C-X-C motif ligand 7 (CXCL7) chemokine, respectively. The expression of these two proteins was increased in WT compared with adjacent normal tissues and normal renal tissues, and increased with increasing clinical stage. In addition, their expression was significantly increased in patients with unfavorable pathological type, lymph node metastasis and vascular involvement compared with the groups with favorable type, and without lymph node metastasis or vascular involvement (P

Sodium butyrate (NaBu), a histone deacetylase inhibitor, has demonstrated anti-tumor effects in several cancers, and is a promising candidate chemotherapeutic agent. However, its roles in nasopharyngeal carcinoma (NPC), an endemic malignant disease in Southern China and Southeast Asia, has rarely been studied. In the present study, MTT assay, colony formation assay, flow cytometry analysis and western blotting were performed to explore the influence of NaBu on NPC cells and its underlying mechanism. NaBu induced morphological changes and inhibited proliferation in 5-8F and 6-10B cells. MTT assay revealed that NaBu was cytotoxic to 5-8F and 6-10B cells in a dose- and time-dependent manner. Furthermore, flow cytometry analysis revealed that NaBu induced obvious cell apoptosis in 5-8F and 6-10B cells due to the activation of the mitochondrial apoptosis axis. In addition, flow cytometry analysis and western blotting demonstrated that NaBu could enhance the Ca2+ influx by promoting store-operated Ca2+ entry (SOCE) in 5-8F and 6-10B cells. Inhibition of SOCE by specific inhibitors or downregulated expression of calcium release-activated calcium channel protein 1 and stromal interaction molecule 1 could counteract the apoptosis of NPC cells induced by NaBu. Thus, the current study revealed that enhanced SOCE and activated mitochondrial apoptosis axis may account for the mechanisms of cytotoxicity of NaBu in NPC cells, and that NaBu serves as a promising chemotherapeutic agent in NPC therapy.

The feasibility and clinical application of single-hole video-assisted thoracoscope in pulmonary peripheral tumors was examined. From March, 2011 to March, 2015, we retrospectively analyzed the clinical data obtained from 32 patients with pulmonary peripheral tumor that received single-hole thoracoscopic surgery. We completed the surgery via a 1.5-cm incision on the seventh or eighth rib in midaxillary line as the observation hole, and a 4.0-5.0-cm incision in the lateral margin of pectoralis major in the fourth or fifth rib in midaxillary line as the operation hole. All the patients had completed the tumor-reductive surgery under single-hole thoracoscope successfully. None required second operation hole or needed a transfer to thoracotomy. Operation time was 40-100 min with an average of 65.78±15.87 min. Intraoperative blood loss was 20-100 ml, with an average of 47.19±26.91 ml. Post-operative chest drainage time was 3-6 days, with an average of 4.22±0.87 days. Hospitalization time after operation was 5-7 days, with an average hospitalization time of 5.97±0.82 days. No patient received a second surgery for pulmonary leak or bleeding and no patient had any complication. All the cases recovered without any problem. In conclusion, for patients with pulmonary peripheral tumor, single-hole video-assisted thoracoscope could further reduce their surgical trauma. The operation was safe and feasible and worthy of wide application.

A number of studies have reported the upregulation and functional roles of Jumonji domain-containing protein 6 (JMJD6) in various types of cancer. However, little is known regarding the clinical significance of JMJD6 in head and neck squamous cell carcinoma (HNSCC), particularly in terms of large-cohort data. In the present study, bioinformatics analysis was performed, using the University of California Santa Cruz Xena Browser and the Gene Expression Profiling Interactive Analysis 2 server, based on the Cancer Genome Atlas HNSCC cohort. In addition, a validation cohort was constructed based on 98 HNSCC cases. JMJD6 overexpression and knockdown, colony-formation, Transwell and cell viability assays were performed. JMJD6 was highly expressed in HNSCC samples and was associated with advanced pathological stage. However, no significant association was observed between JMJD6 expression levels and overall survival or disease-free survival times of patients with HNSCC. Subsequent in vitro assays indicated that overexpression of JMJD6 promoted malignant progression of HNSCC, by regulating epithelial-mesenchymal transition. Nevertheless, JMJD6 overexpression had no significant effects on the viability of HNSCC cells treated with 5-fluorouracil or cisplatin. Thus, it can be concluded that JMJD6 may function as a marker of HNSCC at advanced stage, however with no effect on drug resistance or prognosis. For patients with advanced HNSCC and high JMJD6 expression, rational chemotherapy may be more beneficial than radical surgery, considering their quality of life.

The ubiquitin ligase ring finger protein 5 (RNF5) has previously been associated with the development of breast cancer. Patients with breast cancer and high RNF5 expression have been demonstrated to have a shorter survival time compared with patients with low RNF5 expression. However, the role of RNF5 in human glioma has not been determined. The present study analyzed the role of RNF5 in gliomas using bioinformatics analysis. The results revealed that RNF5 was differentially expressed in non-cancerous brain tissues and different grades of glioma. Furthermore, a high RNF5 expression in patients with glioma was associated with an improved prognosis compared with patients with low expression. Gene Set Enrichment Analysis revealed that RNF5 was particularly associated with 'Wnt signaling pathway', 'apoptosis', 'focal adhesion' and 'cytokine-cytokine receptor interaction' in patients with glioma. Additionally, 4 potential ubiquitination substrates for RNF5 were predicted, including sorting nexin 10, proprotein convertase subtilisin/kexin type 1, leucine rich glioma inactivated 1 and solute carrier family 39 member 12. These findings provided the basis for further investigation on the role of RNF5 in tumors.

The aim of the current study was to investigate the role of enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) in the progression of bladder cancer. Human bladder cancer tissue samples were analyzed by immunohistochemistry, and the association between the clinicopathological parameters and EZH2 expression was analyzed. The proliferation, apoptosis and migration ability of the human bladder cancer cell lines E-J and 5637 with or without the EZH2 inhibitor UNC1999 was investigated. The effect of UNC1999 was further explored in a xenograft model of nude mice. The in vivo and in vitro expression levels of EZH2, janus kinase 2, signal transducer and activator of transcription 3 and their phosphorylated forms were examined by western blotting. The expression levels of EZH2, JAK2 and STAT3 were increased in bladder cancer tissue compared with normal adjacent tissue. Furthermore, the expression of EZH2 was increased in tumors with a higher TNM Classification of Malignant Tumors stage and histological grade compared with tumors with a lower stage and grade. The human bladder cancer cell lines E-J and 5637 treated with UNC1999 demonstrated reduced cell proliferation, apoptosis and migration compared with cells treated without UNC1999. Additionally, EZH2 may promote the proliferation and migration of bladder cancer via the JAK2/STAT3 pathway. EZH2 may serve an important role in the proliferation and migration of human bladder cancer cells, and may aid in the development of novel treatment strategies for bladder cancer.

The present study aimed to investigate the influence of long non-coding (lnc)RNA prostate cancer associated transcript (PCAT)19 on the progression of non-small cell lung cancer (NSCLC). It was determined that PCAT19 expression was upregulated in NSCLC tissues and also predicted poor patient survival rate. Additionally, p53 expression was downregulated in NSCLC specimens, which was negatively correlated with PCAT19 expression. Moreover, in H1993 NSCLC cells, silencing of the PCAT19 gene led to an increase in the expression of p53, whilst conversely, its overexpression led to p53 downregulation. PCAT19 silencing was associated with the decreased proliferation rate of NSCLC cells, while PCAT19 overexpression led to increased proliferation. In addition, p53 overexpression, achieved through the transfection of a p53 expression vector, attenuated the effects of PCAT19 overexpression on cell proliferation. In conclusion, the present study demonstrated that PCAT19 negatively regulates the p53 tumor-suppression pathway, promoting cancer cell proliferation in patients with NSCLC.

Increasing number of microRNAs (miRNAs) have been reported to play an important role in the development and progression of non-small cell lung cancer (NSCLC). In particular, microRNA-497-5p (miR-497-5p) has been proposed as a tumor suppressor miRNA in human cancers. However, the role of miR-497-5p and its potential molecular mechanism associated with NSCLC are less studied. Therefore, the role of miR-497-5p in the pathogenesis of NSCLC was investigated. In the present study, the expression of miR-497-5p was significantly downregulated in NSCLC. Moreover, overexpression of miR-497-5p inhibited the proliferation and invasion of NSCLC cells by suppressing FGF2. In addition, FGF2 was a downstream target of miR-497-5p in NSCLC. FGF2 was upregulated in NSCLC promoting cell proliferation and invasion. Overexpression of FGF2 impaired the inhibitory effect of miR-497-5p in NSCLC. Taken together, these results demonstrate that miR-497-5p is a tumor suppressor miRNA and demonstrate its potential for future use in the treatment of human NSCLC.

The ubiquitin ligase ring finger protein 5 (RNF5) has previously been associated with the development of breast cancer. Patients with breast cancer and high RNF5 expression have been demonstrated to have a shorter survival time compared with patients with low RNF5 expression. However, the role of RNF5 in human glioma has not been determined. The present study analyzed the role of RNF5 in gliomas using bioinformatics analysis. The results revealed that RNF5 was differentially expressed in non-cancerous brain tissues and different grades of glioma. Furthermore, a high RNF5 expression in patients with glioma was associated with an improved prognosis compared with patients with low expression. Gene Set Enrichment Analysis revealed that RNF5 was particularly associated with ‘Wnt signaling pathway’, ‘apoptosis’, ‘focal adhesion’ and ‘cytokine-cytokine receptor interaction’ in patients with glioma. Additionally, 4 potential ubiquitination substrates for RNF5 were predicted, including sorting nexin 10, proprotein convertase subtilisin/kexin type 1, leucine rich glioma inactivated 1 and solute carrier family 39 member 12. These findings provided the basis for further investigation on the role of RNF5 in tumors.

The effect of long non-coding RNA (lncRNA) THOR on proliferation and migration of colon cancer cells was investigated. Lentiviral vector expressing lncRNA THOR shRNA was used to establish colon cancer SW620 lncRNA THOR knockdown cell line (experimental group), and at the same time, a control vector cell line (control group) was established by empty vector virus. Proliferation ability of the two groups was analyzed by CCK8 and EdU methods. Migration ability of the cells was analyzed by Transwell method. Xenograft tumor method was used to analyze the in vivo proliferation ability of the two groups of cells. mRNA levels of lncRNA THOR target genes were analyzed by reverse transcription-quantitative PCR (RT-qPCR). Compared with control cells, the cell proliferation ability of the experimental group was significantly decreased (P

Long non-coding RNA (lncRNA) downregulated in hepatocellular carcinoma (DRHC) is a tumor suppressor in liver cancer. However, the role of this lncRNA in breast cancer has not been investigated. The present study revealed that lncRNA DRHC was downregulated and lncRNA Hox transcript antisense RNA (HOTAIR) was upregulated in tumor tissues compared with adjacent healthy tissues in patients with triple negative breast cancer (TNBC). Expression levels of lncRNA DRHC and lncRNA HOTAIR were negatively correlated in tumor tissues but not in adjacent healthy tissues. The lncRNA DRHC expression level was correlated with tumor size but not tumor metastasis. In vitro overexpression of lncRNA DRHC in TNBC cell lines resulted in decreased expression of lncRNA HOTAIR; however, lncRNA HOTAIR overexpression did not affect the expression level of lncRNA DRHC. Overexpression of lncRNA DRHC inhibited, while overexpression of lncRNA HOTAIR promoted the proliferation of the TNBC cell lines. In addition, lncRNA HOTAIR overexpression attenuated the inhibitory effects of lncRNA DRHC overexpression on cancer cell proliferation. The results obtained in the current study suggested that lncRNA DRHC may inhibit the proliferation of TNBC cells by downregulating the expression of lncRNA HOTAIR.

Cytokine therapy is commonly used for tumor immunotherapy. Although early studies focused directly on the tumor, current investigations are more attentive of the tumor microenvironment. Various immune cells and related cytokines in the tumor microenvironment play an important role in the occurrence and development of tumor. Interleukin (IL)-17 is the characteristic cytokine produced by Th17 cells. IL-17 has been associated with various immune responses. The results of previous studies showed that IL-17 can significantly reduce the size of transplanted tumors in tumor-bearing mice, albeit it has no effect on the survival time of mice. By investigating the effect of IL-17 in the number and distribution of lymphocyte infiltration in tumor tissues, the expression of cytokines and transcription factors associated with the subsets of CD4+T cells in tumor tissues, the distribution of subsets of spleen lymphocyte in tumor-bearing mice, a preliminary investigation of the possible antitumor mechanism of IL-17 was performed. In conclusion, the antitumor effect of IL-17 gene transfection in the colon cancer of mice may be associated with the mechanisms whereby IL-17 gene transfection can change the distribution of different subsets of spleen lymphocytes in mice. IL-17 gene transfection can increase the number of lymphocyte infiltration in tumor tissues. IL-17 gene transfection can promote the high expression of interferon-γ in tumor tissue, while reducing the expression of IL-10 and IL-13 factors, thus exerting an antitumor effect.

The aim of the present study was to examine the effectiveness of curcumin and quercetin in modulating ultrastructural changes during lung carcinogenesis. A total of 24 male laka mice were divided into the normal control, benzo[a]pyrene (BP)-treated, BP+curcumin-treated, BP+quercetin- treated, and BP+curcumin+quercetin-treated groups (n=6 per group). Lung carcinogenesis was induced by a single intraperitoneal injection of BP [100 mg/kg of body weight (b.wt.)]. Curcumin was supplemented to mice at a dose level of 60 mg/kg of b.wt. in drinking water and quercetin was given at a dose level of 40 mg/kg of b.wt. in drinking water. The ultrastructure of BP-treated mice revealed disruptions in cellular integrity together with nuclear deformation and premature mitochondrial aging. Notably, supplementation with phytochemicals individually resulted in improvement of the ultra-histoarchitecture of BP-treated mice although the improvement was much greater with combined supplementation of phytochemicals. Furthermore, BP treatment revealed alterations in lung histoarchitecture, which, however, were improved appreciably following combined supplementation with curcumin and quercetin. The results of the present study show that, combined supplementation with curcumin and quercetin effectively preserved the histoarchitecture as well as ultra-histoarchitecture during BP-induced lung carcinogenesis in mice.

The purpose of the present study was to investigate the effects of upregulating microRNA (miR)-181b expression in tumor-associated macrophages regarding breast cancer cell metastasis and to identify the target gene. Ectopic miR-181b was transfected into MDA-MB-231 and MCF-7 breast cancer cell lines with or without chemokine ligand 18 (CCL18) stimulation. Cell proliferation, migration/invasion and apoptosis rate were investigated. The binding effects of miR-181b to the 3′-untranslated region (UTR) of the nuclear factor (NF)-κB gene were detected with the dual luciferase reporter system. Immunofluorescent staining of the NF-κB key component P65 was performed. The messenger (m) RNA and protein expression of NF-κB induced by CCL18 with or without miR-181b stimulation was evaluated with reverse transcription-quantitative polymerase chain reaction and western blot analysis. When compared with the CCL18-stimulated group, miR-181b mimic-transfected cells exhibited significantly inhibited proliferation and migration, with an increased cell apoptosis percentage in a dose-dependent manner. Furthermore, the luciferase activity was reduced for cells with NF-κB 3′-UTR wild-type that were co-transfected with miR-181b mimics. Immunofluorescent staining of NF-κB demonstrably weakened the P65 signal in stimulated miR-181b mimic cells when compared with parental and CCL18-treated cells. The increased expression level of NF-κB induced by CCL18 in MDA-MB-231 and MCF-7 cells was suppressed by miR-181b mimics. Overexpression of miR-181b suppressed cell survival rate and migration. This overexpression may achieve this goal by regulating the NF-κB pathway in breast cancer cells. Our study demonstrated a potential therapeutic application of miR-181b in the treatment of breast cancer.

Worldwide, human pancreatic cancer is a rare malignancy with a poor prognosis. Long non-coding RNAs (lncRNAs) are known to have a crucial role in cancer occurrence and progression; however, the role of pseudogene-expressed lncRNAs, a major type of lncRNA, have not been thoroughly analyzed in cancer. Therefore, the present study focused on zinc finger protein 91 pseudogene (ZFP91-P). ZFP91-P expression was initially detected in two pancreatic cancer cell lines by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and the highest expression of ZFP91-P was found in the BXPC-3-H cell line. Subsequently, BXPC-3-H cells were transfected with ZFP91-P short hairpin RNA (shRNA) using a plasmid vector and termed shZFP91-P. Cells transfected with negative control plasmid vector were termed shCon. MTT and Transwell assays were performed to analyze the proliferation and migration of BXPC-3-H cells, respectively, and western blotting was used to detect epithelial-mesenchymal transition markers, including vimentin and β-catenin. The present study showed that depletion of ZFP91-P markedly decreased pancreatic cancer cell proliferation and inhibited cell migration capacity. In addition, the expression of β-catenin increased while vimentin expression decreased. The current findings suggest that high expression of ZFP91-P promotes the migration of BXPC-3-H cells and may be a novel marker for early diagnosis for pancreatic cancer.

Malignant mesothelioma is a rare type of cancer, most commonly associated with exposure to asbestos. Mesothelioma of the peritoneum, the membrane lining the abdominal cavity, is extremely rare. The current study reports the case of a 60-year-old female who presented with intestinal fistula, recurrent incisional hernia and abdominal infection, with no history of asbestos exposure, and was diagnosed with clear cell MPM. Computed tomography scans of the abdomen revealed extensive small bowel adhesions and massive peritoneal effusion. Histological examination of biopsy specimens indicated a diagnosis of malignant peritoneal mesothelioma with clear cell morphology. A laparotomy was performed, with subsequent resection of the bowel with fistula. Follow-up examination performed at 1-year post-surgery revealed that the patient was alive and in generally good health.

Wilms' tumors are one of the most common malignant, solid intra-abdominal tumors observed in children. Although potential tumor markers have been found, inflammatory cytokines interfere with the process of specific protein identification. The present study was undertaken to identify post-traumatic stress-related factors of Wilms' tumors and to verify the accuracy of early-stage tumor-specific serum protein markers. Serum samples were screened for differentially-expressed proteins using surface-enhanced laser desorption/ionization-time of flight mass spectrometry (SELDI-TOF-MS). Potential markers were isolated and purified using solid-phase extraction (SPE) and SDS-PAGE. Following enzymatic digestion of the protein samples, the peptide fragments were detected with high performance liquid chromatography-mass spectrometry. The obtained peptide mass fingerprint was searched in the Swiss-Prot protein sequence database via the Mascot search engine. Differentially-expressed proteins were verified using western blot analysis. Differentially-expressed proteins with a mass/charge of 5,816 were screened out using SELDI-TOF-MS, and significant differences between the tumor and control groups, and the trauma and control groups were observed. Target proteins were isolated and purified using SPE and SDS-PAGE. Thioredoxin 1 (Trx1) was found to be differentially expressed. In the serum of children with Wilms' tumors, there was an increase in the level of the post-traumatic stress-related inflammatory factor, Trx1, as compared with the normal control group. Thus, the results of this study indicate that Trx1 presents a potential post-traumatic stress-related factor of Wilms' tumors.

Periosteal osteosarcoma (POS) is a rare primary malignant bone tumor arising from the surface of long bones. In addition, Marfan's syndrome (MFS) is an infrequent hereditary autosomal dominant connective tissue disorder with high penetrance and variable phenotypes, which primarily affects the ocular, skeletal and cardiovascular systems. The present study reported a case of POS and MFS co-occurring in a child. A 6-year-old girl with MFS presented with pain, swelling and deformity in the right thigh following a fall. The patient was diagnosed with a right femoral shaft fracture and underwent open internal fixation surgery at a local hospital. At 2 weeks following surgery, the patient's parents observed increased swelling in the right thigh and thus, revisited the clinic. X-ray examination revealed extensive osteotylus around the fracture site and the clinician decided to remove the internal fixation. Following removal of the implant, aggravated swelling and superficial venous engorgement were observed. The patient was then admitted to Nanfang Hospital, where magnetic resonance imaging was performed, which identified symptoms of an abnormal periosteal reaction with bone erosion, indicating POS. The patient underwent a wide resection of the tumor and the histopathological examination confirmed the diagnosis of POS. No recurrence was identified at 9 months postoperatively. In conclusion, the present case report may result in increased awareness of the possibility of malignant bone tumors in a hereditary patient with osteotylus overgrowth following fracture surgery; in addition, the present case indicated a possible correlation between POS and MFS.

Cancer is the leading cause of death worldwide. The absence of obvious symptoms and insufficiently sensitive biomarkers in early stages of carcinoma limits early diagnosis. Cancer therapy agents and targeted therapy have been used extensively against tissues or organs of specific cancers. However, the intrinsic and/or acquired resistance to the agents or targeted drugs as well as the serious toxic side effects of the drugs would limit their use. Therefore, identifying biomarkers involved in tumorigenesis and progression represents a challenge for cancer diagnosis and therapeutic strategy development. The eukaryotic translation factor 5A (eIF5A), originally identified as an initiation factor, was later shown to promote translation elongation of iterated proline sequences. There are two eIF5A isoforms (eIF5A1 and eIF5A2). eIF5A2 protein consists of 153 residues, and shares 84% amino acid identity with eIF5A1. However, the biological functions of these two isoforms may be significantly different. Recently, it was demonstrated that eIF5Ais widely involved in the pathogenesis of a number of diseases, including cancers. In particular, eIF5A plays an important role in regulating tumor growth, invasion, metastasis and tumor microenvironment. It was also shown to serve as a potential biomarker and target for the diagnosis and treatment of cancers. The present review briefly discusses the latest findings of eIF5A in the pathogenesis of certain malignant cancers and evolving clinical applications.

The present study explored the value of ultrasonography in the diagnosis of primary hepatic carcinoma (PHC) and thyroid carcinoma (TC) by assessing their sonographic features. A total of 426 patients diagnosed with liver space-occupying lesions by ultrasonic examination admitted to Liaocheng People's Hospital from March 2014 to October 2017 were enrolled in this study. These patients were divided into two groups: A total of 226 patients with 237 foci in the PHC group and 200 patients with 216 foci in the benign liver lesion group. During the same period, 367 patients diagnosed with thyroid nodules (382 nodules) by ultrasonic examination were also enrolled in this study. These patients were divided into further two groups: A total of 193 patients with 203 nodules in the TC group and 174 patients with 179 nodules in the benign thyroid nodule group. Two-dimensional and color Doppler ultrasonography were performed on all the patients in the four groups. Differences in the sonographic features such as focus morphology, focus size, internal echo, halo and blood flow distribution were statistically significant between patients in the PHC and the benign liver lesion group (p

Diagnostic value between ultrasound elastography and ultrasound-guided fine needle puncture biopsy in thyroid nodules was compared to provide reference for the selection of thyroid nodule (TN) diagnostic mode. A total of 194 patients with TN, admitted from June 2014 to June 2015, were selected to be treated with ultrasound elastography and ultrasound-guided fine needle puncture biopsy. The ultrasonic elasticity score and results of ultrasound-guided TN puncture were compared with diagnostic results of surgical or ultrasound follow-up for 12 months, and the sensitivity, specificity and accuracy of differentiating and diagnosing TN of the two methods were calculated to compare the clinical diagnostic values. A total of 194 patients were diagnosed with TN 217, including 129 benign and 88 malignant lesions. All the nodules were obtained by effective ultrasound elastography and ultrasound-guided fine needle puncture cytological pathological specimens, and it was diagnosed by ultrasound elastography that there were 75 benign nodules and 142 malignant nodules. It was diagnosed by ultrasound-guided fine needle puncture that there were 112 benign, 78 malignant and 27 uncertain nodules. The specificity and accuracy of ultrasound-guided fine needle puncture in the diagnosis of TN were higher than that of ultrasound elastography and the differences were statistically significant (P0.05), while there was no statistically significant difference between the sensitivity of ultrasound elastography and ultrasound-guided fine needle puncture biopsy in the diagnosis of TN (P0.05). Ultrasound elastography in the diagnosis of TN has a low specificity and the diagnosis of ultrasound-guided fine needle puncture biopsy may have uncertain results. There are some defects in the two diagnostic schemes and their combined application can complement each other's advantages and improve the early diagnostic efficiency of TN.

Mounting evidence has shown that miRNA expression is abnormal in various human cancers. Here, we mainly explored the biological function and the potential mechanisms of miR-1256 in non-small cell lung cancer (NSCLC). The miR-1256 mRNA expression was detected by quantitative real-time PCR and tectonic family member 1 (TCTN1) mRNA expression was detected by immunoblotting. The TCTN1 was identified to be the direct and specific target gene of miR-1256 by luciferase reporter assay. Cell proliferation was examined by methyl thiazolyl tetrazolium assay and migration was detected by transwell assay. MiR-1256 expression was downregulated in NSCLC tissues, whereas the expression of TCTN1 was upregulated, compared with normal tissues. We also found that overexpression of miR-1256 in these NSCLC cell lines inhibited cell proliferation and migration. Furthermore, TCTN1 was identified as a direct target of miR-1256 by luciferase reporter assays. Collectively, these data stated that the inhibitory effect of miR-1256 in NSCLC was realized by upregulating TCTN1, suggesting that miR-1256/TCTN1 axis may play a critical role as NSCLC therapeutic target.

Cancer stem cells (CSCs), which have a close connection with tumor microenvironment, play a pivotal role in tumorigenesis, tumor progression, and metastasis. The inflammatory microenvironment is an essential component of tumor microenvironment. In the recent years, many studies have demonstrated that the inflammatory microenvironment induces the initiation of tumors, and contributes to the process of the progression of tumors, as well as metastasis. In this review, we summarize the relationship between CSCs and inflammatory components, such as inflammatory cytokines (IFNs, TNF, IL-6, IL-17) and inflammatory cells (myeloid-derived suppressor cells, tumor-associated macrophages). To illuminate the key factors that exert important actions in the tumor process would be important to improve the clinical outcome of the treatment for different types of cancer.

Previous studies have demonstrated that microRNAs (miRs) are involved in the carcinogenesis of colorectal cancer (CRC). To the best of our knowledge, the function and regulatory role of miR-532-5p in human CRC remains unknown. The aim of the present study was to determine the role and regulation of miR-532-5p in CRC. Using the reverse transcription-quantitative polymerase chain reaction, it was demonstrated that miR-532-5p was upregulated, whereas runt-related transcription factor 3 (RUNX3) was downregulated in CRC tissues. The upregulated miR-532-5p was associated with the downregulated RUNX3. Furthermore, the two biomarkers were associated with numerous clinicopathological characteristics of CRC, including tumor stage, lymph node involvement, differentiation, vessel invasion and tumor recurrence. The in vitro luciferase reporter assay demonstrated that transfection with miR-532-5p mimic markedly downregulated the RUNX3 mRNA and protein levels, via specific binding to the 5'-untranslated region of RUNX3 in human HT-29 CRC cells. In addition, an MTT assay and a colony formation assay demonstrated that miR-532-5p overexpression led to increased tumor cell viability and colony formation ability of HT-29 cells. In conclusion, the results of the present study indicate that miR-532-5p may function as an oncogenic miRNA by promoting cell growth in human CRC cells, and such promotion is associated with the targeted inhibition of RUNX3.

The apoptosis-stimulating protein of p53 (ASPP) family is a newly identified family protein including ASPP1, ASPP2 and inhibitor of ASPP (iASPP), by which the tumor protein 53 (TP53)-mediated apoptotic process is selectively regulated. Downregulation of ASPP1/ASPP2 and upregulation of iASPP were revealed to be associated with a poor prognosis and metastasis in several types of cancer. However, to the best of our knowledge, the expression of ASPP in colorectal cancer (CRC) has not previously been investigated. The present study analyzed ASPP expression in human CRC tissues with multiple clinical and pathological profiles. A total of 41 patients diagnosed with CRC were enrolled in the present study. The expression of ASPP was detected by immunohistochemistry, immunofluorescence and reverse transcription-quantitative polymerase chain reaction. In addition, the variation in ASPP expression was examined in a number of pathological groups. The associations among ASPP expression, and the expression of TP53, plasma carcinoembryonic antigen (CEA) levels and α-fetoprotein (AFP) levels were also investigated. ASPP1 and ASPP2 expression was significantly reduced, while iASPP expression was elevated in CRC samples compared with expression in adjacent non-cancerous tissues. Downregulation of ASPP1 was detected in the TP53-positive group compared with the TP53-negative group. The increase in iASPP expression was correlated with the grade of malignancy, but not with regional lymph node status or metastases. The expression of ASPP2 was negatively correlated with plasma CEA levels. The results of the present study, not only enrich CRC epidemic and pathological data, but also provide valuable indices for CRC clinical treatment and prognosis.

Cytoplasmic polyadenylation element-binding protein-4 (CPEB4) is involved in several biological processes that are associated with cancer progression. However, it remains unknown whether CPEB4 expression levels are associated with head and neck squamous cell carcinoma (HNSCC). The aim of the present study was to explore the potential function of CPEB4 in HNSCC. The expression of CPEB4 was analyzed in HNSCC from six Gene Expression Omnibus (GEO) datasets. Immunohistochemical staining was conducted to examine CPEB4 protein levels in an HNSCC tissue microarray (TMA). According to the GEO dataset analyses, CPEB4 gene expression was downregulated in HNSCC compared with normal samples (P

Entosis is a homogeneous cell-in-cell phenomenon and a non-apoptotic cell death process. Tyrosine kinase inhibitors have been used in the treatment of prostate cancer and have already demonstrated efficacy in a clinical setting. The present study investigated the role of entosis in prostate cancer treated with the tyrosine kinase inhibitor nintedanib. Prostate cancer cells were treated with nintedanib in vitro and entosis was observed. Mice xenografts were created to evaluate whether nintedanib is able to induce entosis in vivo. The reverse transcription-quantitative polymerase chain reaction, western blotting and immunofluorescence were performed to investigate whether the entosis pathway is induced by nintedanib. It was also investigated whether entosis can contribute to cell survival and progression under nintedanib stress, and nintedanib was revealed to enhance prostate cancer cell entosis. Nintedanib-induced entosis in prostate cancer cells occurred through phosphoinositide 3-kinase/cell division cycle 42 (CDC42) inhibition, followed by the upregulation of epithelial (E-)cadherin and components of the Rho kinase (ROCK) signaling pathway. In addition, nintedanib-resistant cells exhibiting entosis had a higher invasive ability. In addition, in vivo treatment of mice xenografts with nintedanib also increased the expression of E-cadherin and components of the ROCK signaling pathway. Nintedanib can promote entosis during prostate cancer treatment by modulating the CDC42 pathway. Furthermore, prostate cancer cells acquired nintedanib resistance and survived by activating entosis.

Sinonasal hemangiopericytoma (HPC) is a soft tissue tumor of vascular origin. Open surgical methods and endoscopic techniques are considered the standard treatments for sinonasal HPC. However, local recurrences resulting from residual tumors are common. Adjuvant radiotherapy and chemotherapy have also been used to treat HPC, however, the number of studies which have investigated effective adjuvant treatments in the literature are limited. The current study reports a 42-year-old male with recurrent and intracranial invasion of sinonasal HPC, diagnosed in Xuanwu Hospital (Beijing, China). The patient underwent multiple surgeries to remove the tumors, however, no adjuvant therapy was adopted during this period and the tumors reoccurred within 1 year. On admittance to Tangshan People's Hospital (Tangshan, China), the patient presented with limited mouth opening and chewing ability, and hearing loss. Under observation using an electron microscope, HPC usually consists of spindle-shaped cells with elongated nuclei and displays characteristic staghorn-like vascular channels. In the present case, immunohistochemical studies were performed on paraffin-embedded sections of the tumor. The tumor cells expressed CD34, CD68(+/-), epithelial membrane antigen, CD31, α-actin, desmin, CD99, S-100, B-cell lymphoma-2 and Ki-67 (30%), but were negative for creatine kinase. The patient was treated with intensity-modulated radiotherapy and adjuvant chemotherapy, which demonstrated efficacy. No recurrence and metastasis was observed at the 1 year follow-up subsequent to the combined therapy.

The aim of the present study was to compare the tumor volume reduction rate (TVRR), as determined by three-dimensional region-of-interest magnetic resonance volumetry, and Response Evaluation Criteria in Solid Tumors (RECIST) data for predicting the pathological tumor response (PTR) of locally advanced rectal cancer (LARC) following treatment with neoadjuvant chemoradiation (CRT). The current cohort consisted of 105 patients with LARC [clinical tumor stage (cT)3–4 or clinical lymph node stage (cN)+] from a prospective randomized trial who had undergone pre-operative CRT and radical proctectomy. Tumor volumes were measured prior to and following CRT to determine TVRR. Furthermore, receiver operating characteristic (ROC) curves of TVRR and RECIST were constructed to predict the PTR in terms of tumor regression grade (TRG) and downstaging. Values for the area under the ROC curve (AUC) were compared and TVRR cut-off levels were determined. RECIST was used to identify 5 (4.8%) cases of complete response, 44 (41.9%) of partial response, 55 (52.4%) of stable disease and 1 (0.9%) of progressive disease. The mean TVRR was 58.6±24.4%, and a good TRG (0–1) and downstaging occurred in 54 (51.4%) and 59 (56.2%) patients, respectively. In addition, TVRR and RECIST were significantly correlated with TRG and downstaging (P

Cordycepin, also termed 3′-deoxyadenosine, is a derivative of the nucleoside adenosine that represents a potential novel class of anticancer drugs targeting the 3′ untranslated region of RNAs. Cordycepin has been reported to induce apoptosis in certain cancer cell lines, but the effects of cordycepin on human neuroblastoma cells have not been studied. In the present study, an MTT assay revealed that cordycepin inhibits the viability of neuroblastoma SK-N-SH and BE(2)-M17 cells in a dose-dependent manner. In addition, cordycepin increases the early-apoptotic cell population of SK-N-SH cells, as determined by fluorescence-activated cell sorting analysis. The induction of apoptosis in neuroblastoma cells by cordycepin was further confirmed by western blotting, which revealed cleavage of caspase-3 and poly(adenosine diphosphate-ribose) polymerase 1 in the SK-N-SH and BE(2)-M17 cells. Cordycepin also induced the formation of a punctate pattern of light-chain 3 (LC3)-associated green fluorescence in the SK-N-SH cells transfected with a pEGFP-LC3 vector. Furthermore, western blotting revealed cleavage of LC3 A/B in cordycepin-treated neuroblastoma SK-N-SH cells. Taken together, the results indicate that cordycepin significantly increases apoptosis and autophagy in neuroblastoma cells, and may therefore be a drug candidate for neuroblastoma therapy, but requires additional evaluation.

Expression of interleukin-23 receptor (IL-23R) and IL-17 in urinary bladder carcinoma (UBC) was investigated to explore the correlations with prognosis. IL-23/IL-17 axis significantly inhibited the development of inflammatory bowel disease. Thirty patients with UBC were enrolled in Zhengzhou Central Hospital Affiliated to Zhengzhou University from September 2013 to September 2014. Tumor tissue and adjacent healthy tissue were collected, and the levels of IL-23R and IL-17 mRNA were detected by RT-PCR. Thirty healthy people were also selected to serve as normal control group. Serum levels of IL-23R and IL-17 in serum of UBC patients and normal controls were detected by ELISA, and the correlations with clinical features of UBC were analyzed. Pearson's correlation analysis was used to analyze the correlation between IL-23R and IL-17 protein expression. Follow-up study was performed by phone or during patient's visit to out-patient department. Overall survival (OS) and disease-free survival (DFS) curves were plotted by Kaplan-Meier method to analyze the correlation between expression of IL-23R and IL-17 and survival time. ROC curve was used to detect the diagnostic values of IL-23R and IL-17 protein for UBC. Levels of IL-23R and IL-17 mRNA in UBC tissue were 3.26 and 2.65 times higher than those in adjacent tissue (P

Homonoia riparia Lour (Euphorbiaceae) is a known source of herbal medicine in China, and riparsaponin (RSP) is an active constituent isolated from H. riparia. The aim of the present study was to investigate the antitumor effect of RSP on human oral carcinoma cells and its potential underlying molecular mechanism. RSP was isolated from roots of H. riparia and identified using nuclear magnetic resonance. An MTT assay was used to evaluate the cytotoxicity of RSP on human oral carcinoma cells. Subsequently, DAPI staining was performed to investigate the apoptotic effect of RSP. To investigate the potential underlying molecular mechanism of action of RSP, western blotting was performed to determine the expression of cleaved caspase 3/9, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), Bcl-2-associated death promoter (Bad), epithelial cadherin (E-CAD), c-MET, matrix metalloproteinase (MMP)-2 and MMP-9. RSP exhibited a significant anti-proliferative effect on oral carcinoma cells at concentrations between 10 and 200 µg/ml via apoptosis. Following treatment with RSP (20, 40 and 80 µg/ml), expression of cleaved caspase-3 (P

C-terminally truncated hepatitis B virus (HBV) middle size surface proteins (MHBst) has been shown to be a transcriptional activator and may be relevant to hepatocarcinogenesis by transactivating gene expression. In the present study, a pcDNA3.1(−)-MHBst167 vector coding for MHBst truncated at amino acid 167 (MHBst167) was constructed and transfected into the HepG2 hepatoma cell line. mRNA and protein expression of MHBst167 in the cells was detected by reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis. A cDNA library of genes transactivated by the truncated protein in HepG2 cells was made in pGEM-T Easy using suppression subtractive hybridization. The cDNAs were sequenced and analyzed with BLAST searching against the sequences in GenBank. The results showed that certain sequences, such as that of human proto-oncogene c-Myc, may be involved in tumor development. An expression vector pCAT3/c-Myc containing the chloramphenicol acetyltransferase (CAT) gene under the control of a c-Myc promoter was generated, and the transcriptional transactivating effect of MHBst167 on the c-Myc promoter was investigated by RT-PCR and western blotting. MHBst167 was found to upregulate the transcriptional activity of the promoter, as well as transcription and translation of c-Myc. MHBst167 was also shown to transactivate SV40 immediate early promoter, and transcriptionally transactivate the expression of human c-Myc. These findings provide new directions for studying the biological functions of MHBst167, and for a better understanding of the tumor development mechanisms of HBV infection.