MALAT1对子宫内膜癌细胞增殖和凋亡的影响

The effects of MALAT1 on proliferation and apoptosis in endometrial carcinoma

目的探讨长链非编码RNA MALAT1对子宫内膜癌细胞增殖和凋亡的影响及潜在机制。方法以子宫内膜癌RL95-2细胞为研究对象,采用慢病毒载体敲低和过表达MALAT1,利用实时荧光定量PCR检测敲低及过表达效率,通过CCK-8、流式细胞术检测敲低及过表达MALAT1后对RL95-2细胞增殖和凋亡的影响。采用免疫印迹法检测MALAT1表达变化对细胞周期及凋亡相关蛋白CCND1、Bcl-2、Bax表达的影响。结果与空载体对照比较,敲低MALAT1可显著降低细胞增殖能力、诱导细胞凋亡、抑制CCND1、Bcl-2的表达,Bax表达增加,而过表达MALAT1则显著增强细胞增殖和抗凋亡能力。结论长链非编码RNA MALAT1对子宫内膜癌的发生发展有促进作用,抑制MALAT1的表达对子宫内膜癌的治疗有重要意义。

Objective To investigate the effect and potential underlying mechanism of long non-coding RNA MALAT1 on proliferation and apoptosis in endometrial carcinoma cells.Methods Endometrial carcinoma cell line RL95-2 was transfected with lentiviral vectors for knockdown or overexpression of MALAT1,respectively.The expression level of MALAT1 was detected by real-time PCR.CCK-8 assay and flow cytometry were used for analysis of proliferation and apoptosis in RL95-2 cells,respectively.The expression levels of CCND1,Bcl-2 and Bax were determined by Western blotting.Results Knockdown the expression of MALAT1 could significantly reduce the proliferation rate and induce apoptosis in RL95-2 cells.In contrast,MALAT1 overexpression enhanced the proliferation rate and anti-apoptosis ability in RL95-2 cells.Mechanistically,MALAT1 silencing inhibited the expression of CCND1 and Bcl-2,while Bax expression was upregulated.On the contrary,overexpression of MALAT1 enhanced the expression of CCND1 and Bcl-2.Conclusion MALAT1 plays significant roles in the occurrence and development of endometrial carcinoma.Inhibiting the expression of MALAT1 may serve as a therapeutic strategy for the treatment of endometrial carcinoma.