中文摘要：

目的：研究CMTM1-v17（CKLF-like MARVEL transmembrane domain containing family 1-variant17）在正常前列腺及前列腺癌来源细胞系中的表达,初步探索CMTM1-v17对雄激素受体（androgen receptor,AR）转录活性的影响及其作用机制。方法：用免疫组织化学和免疫细胞化学染色的方法分析CMTM1-v17在正常人前列腺组织和前列腺癌来源细胞系中的表达。用荧光素酶报告系统研究CMTM1-v17对AR转录活性的影响及作用机制。结果：CMTM-v17在正常前列腺和前列腺癌来源的LNCaP,Du145和PC3细胞均有表达。荧光素酶报告系统的结果提示在二氢睾酮（5α-dihydrotestosterone,DHT）存在的情况下,将空载体对照组的荧光强度设为100,超表达1μgCMTM1-v17后的相对荧光强度仅为70.8,而超表达2μgCMTM1-v17后的相对荧光强度下降到34.7。当细胞用DHT刺激、同时用组蛋白去乙酰转移酶（histone deacetylase,HDAC）的抑制剂曲古菌素A（trichostatin A,TSA）后,则超表达1μg CMTM1-v17后的相对荧光强度和超表达2μgCMTM1-v17后的相对荧光强度分别从70.8和34.7上升至90.9和86.4。结论：CMTM1-v17在正常前列腺中和前列腺癌来源的细胞系中都有较高丰度的表达,它可能是潜在的AR协同抑制因子,并通过募集HDAC发挥其抑制功能。

英文摘要：

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 immounocytochemistry 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 μg and 2 μg 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 μg and 2 μg 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 deacetylas to inhibit the function of androgen receptor.