OBJECTIVE: To analyze the expression of CMTM1-v17 in normal prostate tissue and prostate carcinoma originated cell lines, and study its impact on the transactivation of androgen receptor and the possible mechanism. METHODS: The expression of CMTM1-v17 in normal prostate tissue was analyzed with immunohistochemistry method. In immunocytochemistry was used to analyze the expression of CMTM1-v17 in prostate carcinoma originated cell lines. Luciferase assay was used to study the impact of CMTM1-v17 on the transactivation of AR and its mechanism. RESULTS: The results of immunohistochemistry showed that CMTM1-v17 was highly expressed in prostate. In prostate cancer originated cell lines, CMTM1-v17 could also be detected in prostate cancer originated cell lines PC3, Du145 and LNCaP. And the results of luciferase implied that the relative luciferase activity of the PC3 cells transfected with 1 microg and 2 microg pCDI-CMTM1-v17 plasmids separately were 70.8 and 34.7, compared with the control set as 100. When trichostatin A, the inhibitor for histone deacetylase, was used, the repression of androgen receptor could be recovered with trichostatin A treatment,for the relative luciferase activity of the PC3 cells transfected with 1 microg and 2 microg pCDI-CMTM1-v17 plasmids and treated with 100 nmol/L trichostatin A rebound to 90.9 and 86.4. CONCLUSION: CMTM1-v17 is highly expressed in both normal prostate and prostate carcinoma originated cell lines. It may recruit histone deacetylase to inhibit the function of androgen receptor.
OBJECTIVE: To analyze the expression of CMTM1-v17 in normal prostate tissue and prostate carcinoma originated cell lines, and study its impact on the transactivation of androgen receptor and the possible mechanism. METHODS: The expression of CMTM1-v17 in normal prostate tissue was analyzed with immunohistochemistry method. In immunocytochemistry was used to analyze the expression of CMTM1-v17 in prostate carcinoma originated cell lines. Luciferase assay was used to study the impact of CMTM1-v17 on the transactivation of AR and its mechanism. RESULTS: The results of immunohistochemistry showed that CMTM1-v17 was highly expressed in prostate. In prostate cancer originated cell lines, CMTM1-v17 could also be detected in prostate cancer originated cell lines PC3, Du145 and LNCaP. And the results of luciferase implied that the relative luciferase activity of the PC3 cells transfected with 1 microg and 2 microg pCDI-CMTM1-v17 plasmids separately were 70.8 and 34.7, compared with the control set as 100. When trichostatin A, the inhibitor for histone deacetylase, was used, the repression of androgen receptor could be recovered with trichostatin A treatment,for the relative luciferase activity of the PC3 cells transfected with 1 microg and 2 microg pCDI-CMTM1-v17 plasmids and treated with 100 nmol/L trichostatin A rebound to 90.9 and 86.4. CONCLUSION:CMTM1-v17 is highly expressed in both normal prostate and prostate carcinoma originated cell lines. It may recruit histone deacetylase to inhibit the function of androgen receptor.