肿瘤抑制基因DBC2抑制乳腺癌MDA-MB-435S细胞增殖并诱导凋亡

DBC2 negatively regulates the proliferation of breast cancer cells and induces apoptosis

目的观察肿瘤抑癌基因DBC2（deletioninbreastcancer2）的过表达在乳腺癌MDA—MB-435S细胞中的功能。方法野生型DBC2基因的真核表达载体pEBG—DBC2瞬时转染MDA—MB-435S细胞72h，噻唑蓝（MTF）比色法绘制DBC2转染前后MDA—MB-435S细胞生长曲线；流式细胞术检测DBC2的瞬时过表达对MDA—MB-435S细胞周期的影响，TUNEL方法原位检测DBC2的过表达诱导MDA—MB-435S细胞凋亡。结果DBC2基因在MDA—MB-435S细胞中的过表达可显著抑制该细胞的增殖，同时DBC2基因的过表达可诱导该乳腺癌细胞周期的G，期阻滞（64．05％比71．72％）和细胞凋亡（0．09％比5．29％）。TUNEL实验证实DBC2诱导MDA—MB-435S细胞凋亡的百分比为8％。结论DBC2基因体外抑制乳腺癌细胞生长的功能，可能通过细胞周期G，期停滞，以及诱导细胞凋亡等机制实现。

Objective To gain insight into the biological function of DBC2 in MDA-MB-435S breast cancer cell line in vitro. Methods Transient DBC2 over-expression in MDA-MB-435S cell line was generated by lipofectamine2000 transfection. MTT assay was performed to verify the function of growth inhibition of DBC2 over-expression. The effects of transient DBC2 over-expression was checked by flow cytometry. TUNEL was used to evaluate the apoptosis induced by DBC2. Results The over-expression of DBC2 could significantly inhibit the proliferation of MDA-MB-435S cells and the percentage of inhibition was from 25.95% to 36.43%. Transient over-expression of DBC2 could also induce cell cycle G1 arrest （64.05% vs. 71.72%）. Moreover, TUNEL assay showed that the percentage of apoptosis was about 8%. Conclusion Transient over-expression of DBC2 in vitro could inhibit the growth of breast cancer cells, possibly through the mechanisms of inducing G1 cell cycle arrest and apoptosis.