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肿瘤抑制基因DBC2在乳腺癌中的表达和对T47D细胞增殖的抑制作用 被引量:3

Expression of tumor suppressor gene DBC2 in breast cancer and functional analysis of DBC2 in T47D cells
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摘要 目的探讨抑癌基因DBC2在乳腺癌中的表达和抑制乳腺癌T47D细胞系增殖的可能机制。方法逆转录-聚合酶链反应(RT-PCR)方法检测原发性乳腺癌标本中DBC2基因的缺失表达情况;检测DBC2的瞬时表达对T47D细胞增殖和细胞周期的影响,以及对关键细胞周期蛋白表达的作用。结果在37.5%的原发性乳腺癌标本中DBC2的表达缺失;DBC2在T47D细胞中的瞬时表达使细胞周期出现G1期阻滞,DBC2瞬时表达48h后,处于G1期的百分比为66.29%,而对照组为57.64%;DBC2的表达不能抑制CyelinE和C-Myc的表达,但能显著的抑制Cyclin D1的表达。结论DBC2的缺失表达与原发性乳腺癌的发生关系密切,DBC2的表达可抑制体外乳腺癌细胞的生长,可能通过抑制Cyclin D1的表达并使细胞停滞于G1期等机制实现。 Objective To study the expression of tumor suppressor gene DBC2 in primary breast cancer and the probable mechanisms by which DBC2 inhibits the proliferation of T47D breast cancer cell line. Methods RT-PCR was performed to detect the expression of DBC2 mRNA in primary breast cancer biopsy samples; transient DBC2 expression in T47D cell line which was DBC2-deficient was generated by lipofectamine 2000 transfection; the effects of transient DBC2 expression was examined by flow cytometry; moreover,Western blot was used to evaluate the cell cycle related protein expression. Results The expression of DBC2 was deficient in 37.5% primary breast cancer biopsy samples. DBC2 could significantly induce cell cycle G1 arrest in vitro. DBC2 could also decrease the expression of cyclin D1 but not cyclin E and c-myc. Conclusion There was a close relationship between DBC2 deficiency and primary breast cancer tumogenesis. Transient expression of DBC2 in vitro could inhibit the growth of breast cancer cells, possibly through the mechanisms of decreasing the expression of cyclin D1 and inducing Gl cell cycle arrest.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2008年第1期15-17,共3页 Chinese Journal of Experimental Surgery
基金 国家自然科学基金资助项目(30400432)
关键词 乳腺肿瘤 基因表达 细胞周期 Breast neoplasm Gene expression Cell cycle
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