miR-630通过靶向BMI1抑制乳腺癌细胞增殖的作用机制研究

Study on mechanism of miR-630 inhibiting the biological behavior of breast cancer cells by targeting the expression of BMI1

目的探讨miR-630通过靶向BMI1对乳腺癌细胞的生物学行为影响及其作用机制。方法倒置显微镜下观察检测MiR-630诱导乳腺癌细胞凋亡并抑制增殖的情况;流式细胞术和集落形成实验检测miR-630对细胞周期和集落形成的影响;双荧光素酶实验检测miR-630和BMI1在乳腺癌细胞中的相互作用;流式细胞术和集落形成实验检测BMI1对miR-630在细胞周期和集落形成过程中的逆转作用。结果 miR-630可以抑制乳腺癌细胞的增殖,促进其凋亡进程;miR-630的异位表达可以诱导细胞凋亡和细胞周期阻滞,抑制乳腺癌细胞的克隆增殖行为;BMI1是miR-630的直接靶基因,miR-630可以直接调控BMI1的表达活性;BMI1异位恢复时,miR-630的增殖和集落形成的抑制能力也得到了部分恢复。结论 miR-630在乳腺癌的发生发展过程中起重要作用,可以和BMI1相互影响调控乳腺癌细胞的生物学行为。

Objective To investigate the mechanism of miR-630 inhibiting the biological behavior of breast cancer cells by targeting the expression of BMI1. Methods The breast cancer cell apoptosis induced by miR-630 and its inhibition on proliferation of breast cancer cells were observed and detected by the inverted microscopy. The effect of miR-630 on cell cycle and colony formation were detected by flow cytometry and colony formation assay. Dual luciferase assay was used to detect the interaction of miR-630 and BMI1 in breast cancer cells. Flow cytometry and colony formation assay were used to detect the reversal effect of BMI1 on miR-630 in cell cycle and colony formation. Results miR-630 could inhibit theproliferation and promote the apoptosis of breast cancer cells; ectopic expression of miR-630 could induce apoptosis and cell cycle arrest and inhibit the cloning and proliferation of breast cancer cells. BMI1 is a direct target gene of miR-630,while miR-630 can directly regulate the expression of BMI1 activity. During BMI1 ectopic recovery,miR-630 proliferation and colony formation inhibition ability has also been partially restored. Conclusion miR-630 plays an important role in the incidence and progression of breast cancer. It can interact with BMI1 to regulate the biological behavior of breast cancer cells.