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Myosin heavy chain 11 (MYH11), encoded by the MYH11 gene, is a protein that participates in muscle contraction through the hydrolysis of adenosine triphosphate. Although previous studies have demonstrated that MYH11 gene expression levels are downregulated in several types of cancer, its expression levels have rarely been investigated in lung cancer. The present study aimed to explore the clinical significance and prognostic value of MYH11 expression levels in lung cancer and to further study the underlying molecular mechanisms of the function of this gene. The Oncomine database showed that the MYH11 expression levels were decreased in lung cancer compared with those noted in the normal lung tissue (P<0.05). Kaplan-Meier plotter results revealed that the decreased MYH11 expression levels were correlated with poor prognosis in lung cancer patients. Among the lung cancer cases with gene alteration of MYH11, mutation was the most common of all alteration types. Coexpedia and Metascape analyses revealed that the target genes were primarily enriched in 'muscle contraction', 'contractile fiber part', 'actin cytoskeleton' and the 'adherens junction'. These results indicated that MYH11 is a potential novel drug target and prognostic indicator of lung cancer. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the molecular mechanisms and effect of Beclin-1 on autophagy, proliferation and apoptosis in the colorectal cancer (CRC) HCT116 and SW620 cells. Beclin-1 was silenced by RNA interference (RNAi) in HTC116 and SW620 cells. Reverse transcription-polymerase chain reaction and western blot were used to measure the expression of Beclin-1. The percentage of apoptotic cells was analyzed by cell counting kit-8 (CCK-8) and flow cytometry (FCM). Cell cycle and cell proliferation were analyzed by FCM and the MTT assay. The present study created 3 groups in the two cell lines, consisting of the targeting siRNA (TS) group, in which Beclin-1 was partially silenced, non-specific siRNA (NS) group and control group (CG; without transfection). By siRNA transfection, the mRNA and protein level of Beclin-1 in the TS group were significantly inhibited compared with the NS group and CG (P<0.05). After 0, 24, 48 and 72 h, the survival rate of the cells in the TS group was significantly decreased compared with the survival rate of the cells in the NS group and CG, as detected by CCK-8 methods (P<0.05). FCM and MTT results showed the apoptotic rate of the cells in the TS group was significantly decreased compared with the rate in the NS group and CG (P<0.05), and the proliferation of the cells in the NS group was evidently increased compared with the CG. In conclusion, Beclin-1 played an important role in regulating autophagy, proliferation and apoptosis in HCT116 and SW620 cells. The inhibition of Beclin-1 by RNAi suppressed the autophagic activity and proliferation, but promoted apoptosis in CRC cells. Beclin-1 was the new target of gene therapy for CRC. [ABSTRACT FROM AUTHOR]

The aim of the present study was to examine and discuss the association between multidrug resistance 1 gene (MDR1) of gastrointestinal tumors, the expression of P-glycoprotein and resistance to chemotherapeutic drugs. In this study, 126 cases of patients with gastrointestinal tumors admitted to hospital from February 2013 to February 2015 were selected. The expression levels of MDR1 gene were obsreved in the control population and patients before and after treatment by fluoresecent quantitative PCR. The protein expression level of P-glycoprotein was determined using western blotting and enzyme-linked immunosorbent assay. In addition, drug resistance was assessed by ATP-TCA chemosensitivity experiments. The results showed that before treatment, the expression of mRNA in MDR1 of tissues of gastrointestinal tract of the 126 cases was 108-fold larger than that of the gastrointestinal tract of the controls (p<0.05), P-glycoprotein was 87-fold larger than the expression level of the controls (p<0.05). The sensitivity of 126 tumor tissues to different chemotherapeutic drugs was determined, and the results showed that most of the tumor tissues were sensitive to chemotherapeutic drugs, and the sensitivity rate reached 96.4%. Following chemotherapy, the expression of mRNA in MDR1 of tumor tissues and the expression of P-glycoprotein decreased (p<0.05). In conclusion, the MDR1 gene and P-glycoprotein have a positive correlation with the occurrence of gastrointestinal tumors, and a negative correlation between the MDR1 gene and P-glycoprotein with resistance of chemotherapeutic drugs. Therefore, the MDR1 gene and P-glycoprotein can be used as references in the identification and diagnosis of gastrointestinal tumors. [ABSTRACT FROM AUTHOR]

Cancer metastasis remains responsible for the vast majority of cases of cancer-related morbidity and mortality. Metastasis, by its definition, is the spread of cancer from the primary site to the distant tissues. Advancing the scientific and clinical understanding of cancer metastasis is a high priority. The prerequisite requirement for pathological consistency may be compromised during metastasis. The present study reports the case of a cancer patient with different pathological types. The patient presented with pain in the neck and right hip, as well as weight loss. He underwent whole-body positron emission tomography-computed tomography, which identified a mass in the lung and abnormal metabolism of the bone. Biopsies of the ilium and lung were performed and he was shown to have lung adenocarcinoma and bone squamous carcinoma. The morphology and immunohistochemical patterns were completely different, while each lesion harbored an identical genetic profile. The bone lesion was identified to be a metastasis from the lung cancer. The patient was prescribed an epithelial growth factor receptor inhibitor, which resulted in a partial response in the lung mass and alleviation of the patient's bone pain. Through this case study, we advocate the importance of using genetic testing in addition to pathological assessment. [ABSTRACT FROM AUTHOR]

Sesquiterpenoids are a major type of compound found in Solanum lyratum (S. lyratum). The present study aimed to investigate whether sesquiterpenoids from S. lyratum demonstrated cytotoxicity against the MCF-7, HCT-8, A-549, SGC-7901 and BEL-7402 cell lines, and the mechanism of solajiangxin H and lyratol D, which exhibited high cytotoxicity against SGC-7901 cells (half maximal inhibitory concentration, IC50=4.8 and 5.9 µg/ml), was associated with mitochondria-mediated apoptosis. The results of the Cell Counting Kit-8 assay indicated that 15 sesquiterpenoids had cytotoxicity against the aforementioned cultured cells. The results of DAPI staining and western blot analysis, used to study the anticancer mechanisms of solajiangxin H and lyratol D in SGC-7901 cells, suggested that solajiangxin H and lyratol D induced the apoptosis of SGC-7901 cells significantly (P<0.01), downregulated the expression of the antiapoptotic proteins B-cell lymphoma (Bcl)-2 and survivin, and upregulated the expression of the proapoptotic proteins Bcl-2-like protein 4, second mitochondria-derived activator of caspase, cleaved (c)-caspase-3 and c-caspase-9. The present study therefore demonstrated that 15 sesquiterpenoids from S. lyratum exhibited anticancer activity in MCF-7, HCT-8, A-549, SGC-7901 and BEL-7402 cells, and that the anticancer mechanisms of solajiangxin H and lyratol D may be associated with mitochondria-mediated apoptosis. Additionally, the present study provides evidence in support of the hypothesis that S. lyratum may be a promising candidate for the development of novel cancer therapies. [ABSTRACT FROM AUTHOR]

Cholangiocarcinoma is one of the most aggressive types of malignancy, and is associated with poor patient prognosis. Recent findings suggest that a decrease in pleckstrin homology-like domain family A, member 1 (PHLDA1) expression is significant in the induction of cell migration and tumor invasion. The clinicopathological significance of the expression of PHLDA1, and its potential correlation with the expression of CD133 in cholangiocarcinoma have remained to be elucidated. In the present study, PHLDA1 protein expression was investigated by immunohistochemical analysis of 218 cholangiocarcinoma tissue samples, as well as 30 para-neoplastic and 20 normal bile ducts. The expression status of PHLDA1 and CD133 was determined, and these results were analyzed against the age, gender, tumor location and size, histological grade, clinical stage and overall mean survival time of the patients. The expression of PHLDA1 protein was markedly decreased in 35.3% of cholangiocarcinomas, compared with that of the para-neoplastic and normal cholangiocytes. Carcinomas with loss of expression of PHLDA1 were signifi- cantly correlated with the tumor site (P=0.001), histological grade (P=0.020) and clinical stage (P=0.0001), but not with age (P=0.085), gender (P=0.456 ) or size (P=0.413), respectively. Kaplan-Meier survival analysis indicated that the loss of expression of PHLDA1 was significantly correlated with the overall survival time (Log rank=193.861; P=0.0001). Furthermore, the expression of PHLDA1 was found to be inversely correlated with the expression of CD133 (γ=-0.142; P=0.036). These findings suggested that the decreased expression of PHLDA1 may be significant in the carcinogenesis and progression of cholangiocarcinoma, and may represent a novel adjunct marker of disease prognosis. [ABSTRACT FROM AUTHOR]

Mediator Complex Subunit 12 (MED12) is a subunit of the mediator complex, which is believed to regulate global, as well as gene-specific, transcription. It has been reported that MED12 is mutated at high frequency in hysteromyoma. Recent studies have also shown that MED12 presents with different mutation frequencies in hysteromyoma patients of different populations. However, there are few studies with regard to the MED12 gene mutation in hysteromyoma patients in the Chinese Han population. In the present study, the MED12 mutations of 171 patients with hysteromyoma were analyzed; the results showed that 93 patients exhibited different MED12 mutations, including 131G→T, 131G→A, 130G→A, 146C→T, 130G→A, 130G→C, 128A→C, 130G→T, 127Ins27, 118_132Del15, 117_134Del18, 131_148Del18 and 141_165Del15. The mutation frequency was similar to that found in individuals of African descent or individuals of other non-Caucasian ethnicities, and lower than that in the Finnish or North American populations. Further analysis of 141 patients whose hysteromyoma was measured showed that the mutation frequency of MED12 in patients with large hysteromyomas was significantly lower than that in those with small hysteromyomas. These results suggested that MED12 mutation was important in the development of hysteromyomas in the Chinese Han population and that the size of the hysteromyoma may negatively correlate with the mutation frequency of MED12. This study supplemented current information on MED12 mutations in different races and may aid in developing personalized diagnoses for patients with hysteromyoma in the future. [ABSTRACT FROM AUTHOR]

Guan Chang Fu Fang (GCFF) is a natural compound, which is extracted from three medicinal plants, Agrimonia pilosa Ledeb., Patrinia scabiosaefolia and Solanum nigrum L. GCFF has demonstrated clinical efficacy in the treatment of colon cancer. At present, 5-fluorouracil (5-FU) is the primary active chemotherapeutic agent used for treating colon cancer. Using median-effect and apoptosis analyses, fluorescence microscopy and western blotting, the present study analyzed the association between GCFF and 5-FU in the human colon adenocarcinoma LoVo cell line. The effect of GCFF on the expression of chemotherapeutic agent-associated genes was also investigated. The results of the synergistic analysis revealed that GCFF exhibited a significant effect upon 5-FU-associated cytotoxicity within the LoVo cell line. This effect was observed over a broad dose-inhibition range (5-95%), but was particularly significant in the lower concentrations. The flow cytometry results revealed that low doses of GCFF or 5-FU induced S -phase arrest, as did a low-dose combination of the two drugs. After 48 h, GCFF significantly suppressed the expression levels of the chemotherapeutic agent resistance-associated genes within the colon cancer cells. The western blot analysis revealed that the combined effects of 5-FU and GCFF were due to a regulation of the B-cell lymphoma-2 family of proteins. The findings of the present study suggested that GCFF, when combined with 5-FU, has the potential to be a novel, chemotherapeutic compound for the treatment of colon cancer. [ABSTRACT FROM AUTHOR]

Few cases of testicular metastases from prostate carcinoma have been reported, and asymptomatic metastases of prostate carcinoma to both the testis and epididymis are extremely rare. The current study presents the case of a 69-yearold male with testicular and epididymal metastases from prostate carcinoma. The patient was admitted to The First Hospital of Shijiazhuang with a 2-year history of lower urinary tract symptoms. Digital rectal examination revealed an enlarged multinodular prostate, and the serum prostate-specific antigen (PSA) level was >100 ng/ml. Magnetic resonance imaging showed prostate carcinoma with seminal vesicle involvement. A prostate biopsy showed prostate gland adenocarcinoma. The Gleason score was 3+3. The immunohistochemistry results were as follows: Prostatic acid phosphatase (+++), PSA (+++), P504s (+++), p63 (-) and cytokeratin 34βE12 (-), with a Ki-67 of ~5%. The patient was treated with a bilateral orchiectomy. The testicular pathology showed that the right testis and epididymis were invaded with metastatic adenocarcinoma. The left testis and epididymis were normal. The patient was treated with conventional flutamide endocrine therapy. At present the patient remains in a stable condition after 24 months of follow-up. [ABSTRACT FROM AUTHOR]