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BACKGROUND: Prostate cancer is one of the most common cancer types both in western and eastern countries, involving mostly elder men. The mechanisms underlying the prostate cancer development remain unclear. Prostate-specific antigen (PSA) is the only well accepted marker for prostate cancer diagnosis and prognosis. The diagnosis and treatment of prostate cancer are facing big challenges. Here, we evaluated the expression of Dipeptidyl peptidase IV (CD26/DPPIV) and C-X-C chemokine receptor type 4 (CXCR4), two known cancer-related molecules but without clear data on prostate cancer population, and their correlation with clinical parameters in prostate cancer tissue array. To explore the correlation of CD26 and CXCR4 expression in prostate carcinoma and their relationship with clinical parameters. MATERIALS AND METHODS: We immunohistochemically stained the tissue array containing samples from 36 cases with prostate cancer with CD26 and CXCR4 antibodies. Then we analyzed the expression of CD26 and CXCR4 and its relationship with clinical parameters. We used immunohistochemical staining to evaluate the expression of CD26 and CXCR4 in a set of tissue array containing 36 cases of prostate cancers and eight peritumoral normal prostatic tissues. The data were statistically analyzed with Statistical Package for Social Sciences (SPSS) 16.0 software. The difference between parameters was compared with nonparametric test and correlation analysis was performed with Spearman test. P < 0.05 was considered as significant. RESULTS: We found both CD26 and CXCR4 expression were higher in cancer tissue than in normal tissues. CD26 and CXCR4 levels were correlated with each other. Moreover, CD26 was correlated with PSA level, tumor residue, cancer stage, and tumor size in the studied samples. CONCLUSION: Our data indicate that CD26 may be a good indicator for cancer behaviors of prostate cancer in clinic.
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CONTEXT: Se-methylselenocysteine (MSC), as a chemopreventive agent, shows antitumor effects in some cancer models, but its mechanism is still unclear. AIMS: This study is to explore whether MSC induces apoptosis in prostate cancer (PCa) cells DU145 through connexin 43 (Cx43) activation. SETTINGS AND DESIGN: The experiment was performed in a PCa cell line model DU145 and using a series of biological assay methods to investigate the regulating pathway from MSC through Cx43 to downstream molecules, demonstrating an important role of Cx43 in PCa development and as a potential treatment target. MATERIALS AND METHODS: The human PCa cell line DU145 was used as a model. The effects of MSC on Cx43 expression were examined by reverse transcription-polymerase chain reaction, western blot; effects on cell growth and proliferation were determined by WST-1 and colony formation assay; small interfering ribonucleic acid was used to evaluate the direct contribution of Cx43 to cancer cell apoptosis. STATISTICAL ANALYSIS USED: Student's t-test was used to calculate the difference between the groups in SPSS software. RESULTS: Results showed that MSC inhibited the growth and colony formation of the DU145 cells; MSC induced cell apoptosis by increasing Cx43 expression at messenger ribonucleic acid and protein levels; MSC decreased B-cell lymphoma-2 (Bcl-2) and increased bad levels of DU145 cells. CONCLUSIONS: As a conclusion, MSC exerts pro-apoptosis effects through increasing Cx43 expression, which in turn down-regulates Bcl-2 and up-regulates bad expression.