miR-128通过RECK靶向作用影响乳腺癌细胞的生物学行为

miR-128 affects biological behavior of breast cancer cells through the targeting of RECK

目的探讨miR-128通过RECK靶向作用影响乳腺癌细胞的生物学行为及其作用机制。方法 Western blot检测miR-128在细胞株中的表达情况及慢病毒转染效率;流式细胞术检测miR-128对乳腺癌细胞凋亡行为的影响;双荧光素酶实验检测miR-128和RECK在乳腺癌细胞中的相互作用;流式细胞术实验检测RECK对miR-128在乳腺癌细胞周期和集落形成过程中的逆转作用。结果 MCF-7细胞中miR-128的表达量是NC组细胞的3. 05倍,慢病毒转染效率明显; miR-128通过诱导细胞凋亡和抑制细胞周期进程来抑制MCF-7细胞的生长; RECK是miR-128的直接靶基因,miR-128可以直接调控RECK的表达活性; RECK异位恢复时,miR-128对乳腺癌细胞的凋亡和细胞周期的抑制也得到了部分恢复。结论 miR-128在乳腺癌的发生发展过程中起重要作用,可以和RECK相互影响调控乳腺癌细胞的生物学行为,提示miR-128和RECK可能成为乳腺癌的潜在治疗靶标。

Objective To investigate the biological behavior of breast cancer cells induced by miR-128 targeting RECK and its possible mechanism. Methods The expression of miR-128 in cell lines and transfection efficiency of lentiviral were detected by Western blot. Flow cytometry was used to detect the effect of miR-128 on the apoptosis of breast cancer cells. The dual luciferase assay was used to detect the interaction of miR-128 and RECK in breast cancer cells. Flow cytometry was used to detect the reversal effect of RECK on miR-128 in the cell cycle and colony formation of breast cancer cells. Results The expression of miR-128 in MCF-7 cells was 3. 05 times that of NC cells,and the lentiviral transfection efficiency was obvious. miR-128 inhibits the growth of MCF-7 cells by inducing apoptosis and inhibiting cell cycle progression. RECK was the direct target of miR-128,and miR-128 directly regulated the expression of RECK. RECK ectopic recovery,miR-128 on breast cancer cell apoptosis and cell cycle inhibition had also been partially restored. Conclusion miR-128 plays an important role in the development and progression of breast cancer. It can interact with RECK to regulate the biological behavior of breast cancer cells,which suggests that miR-128 and RECK may be the potential therapeutic targets of breast cancer.