摘要
目的:探讨长链非编码RNA(LncRNA)CCAT1对子宫内膜癌细胞增殖、凋亡和磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)信号通路影响,阐明CCAT1在子宫内膜癌生长中的作用及可能机制。方法:将HEC-1-A细胞分为空白对照组(BC)、阴性对照组(NC)和CCAT1-siRNA组,CCAT1-siRNA组细胞转染CCAT1-siRNA,NC组转染阴性对照siRNA,BC组不转染。RT-PCR测定细胞中CCAT1水平。CCK8测定HEC-1-A细胞增殖情况。流式细胞术测定HEC-1-A细胞凋亡。Western blot测定HEC-1-A细胞PCNA、活化的cleaved caspase 3、Bax、Bcl-2、PI3K、AKT、p-AKT蛋白水平。结果:HEC-1-A细胞中CCAT1水平(2.15±0.24)高于T-HESC细胞(1.00±0.13)(t=11.147,P<0.001)。与BC组和NC组相比,CCAT1-siRNA组HEC-1-A细胞中CCAT1水平降低(P<0.001),细胞增殖率降低(P<0.001),细胞凋亡率降低(F=112.080,P<0.001),PCNA和Bcl-2蛋白水平降低(P<0.001),cleaved caspase 3和Bax蛋白水平升高(P<0.001),PI3K和p-AKT蛋白水平降低(P<0.001)。BC组和NC组HEC-1-A细胞中各指标差异无统计学意义(P>0.05)。结论:沉默子宫内膜癌细胞中CCAT1可抑制细胞增殖、促进细胞凋亡,其机制可能与沉默CCAT1可抑制PI3K/AKT信号通路有关。
Objective:To investigate effects of long-chain non-coding RNA(LncRNA)CCAT1 on proliferation,apoptosis and phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)signaling pathway in endometrial cancer cells,and to elucidate the role of CCAT1 in growth of endometrial cancer and its possible mechanism.Methods:HEC-1-A cells were divided into blank control group(BC),negative control group(NC)and CCAT1-siRNA group.Cells of CCAT1-siRNA group were transfected with CCAT1-siRNA,cells of NC group were transfected with negative control siRNA,cells of BC group were not transfected.Level of CCAT1 in cells was determined by RT-PCR.CCK8 was used to determine proliferation of HEC-1-A cells.Apoptosis of HEC-1-A cells was measured by flow cytometry.PCNA,activated cleaved caspase 3 Bax,Bcl-2,PI3K,AKT,p-AKT protein levels of HEC-1-A were determined by Western blot.Results:Level of CCAT1 in HEC-1-A cells(2.15±0.24)was higher than that in T-HESC cells(1.00±0.13)(t=11.147,P<0.001).Compared with BC group and NC group,CCAT1 levels were decreased(P<0.001),proliferation rate of cells was decreased(P<0.001),apoptosis rate was decreased(F=112.080,P<0.001),PCNA and Bcl-2 protein levels were reduced(P<0.001),cleaved caspase 3 and Bax protein levels were elevated(P<0.001),PI3K and p-AKT protein levels were reduced(P<0.001)in HEC-1-A cells in CCAT1-siRNA group.There were no significant difference in the indexes of HEC-1-A cells between BC group and NC group(P>0.05).Conclusion:Silencing of CCAT1 in endometrial cancer cells can inhibit cell proliferation and promote apoptosis,whose mechanism may be related to that silencing of CCAT1 can inhibit the PI3K/AKT signaling pathway.
作者
李林
刘晶
王景
杨睿
LI Lin;LIU Jing;WANG Jing;YANG Rui(Department of Obstetrics and Gynecology,the First Hospital of Hebei Medical University,Shijiazhuang 050000,China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2020年第22期2737-2741,共5页
Chinese Journal of Immunology
基金
河北省卫健委医学科学研究项目(20190431)。
