lncRNA AK126393通过PI 3K/Akt通路调节结直肠癌细胞的增值与凋亡

lncRNA Ak126393 Modulates Proliferation and Apoptosis of Colorectal Cancer Cells through the PI 3K/Akt Pathway

目的探索长链非编码RNA(long non-coding RNA,lncRNA)AK126393在人结直肠癌细胞中的作用机制。方法荧光定量PCR(qRT-PCR)检测正常结肠组织细胞系与结直肠癌细胞系中lncRNA AK126393表达,选取最低表达细胞系进行转染lncRNA AK126393过表达质粒和阴性对照(NC),采用CCK-8法检测细胞活力,流式细胞术检测细胞周期与凋亡,Western blot法检测Bcl2、Bax、PI 3K、P-PI 3K、Akt、P-Akt和LC3蛋白表达。结果lncRNA AK126393在结直肠癌细胞系中呈现低表达,其中SW480细胞表达最低;过表达质粒转染SW480细胞后lncRNA AK126393相对表达水平显著升高;细胞增值能力显著降低,细胞凋亡水平增加;Western blot法检测结果显示Bcl2、LC3-Ⅱ、P-PI 3K、P-Akt蛋白表达明显升高,Bax和LC3-Ⅰ蛋白表达明显降低,PI 3K和Akt蛋白表达无明显变化。结论lncRNA AK126393可以通过抑制PI 3K/Akt信号通路激活实现抑制结直肠癌细胞增殖、促进细胞凋亡以及引起细胞自噬的作用。

Objective To explore the mechanism of long non-coding RNA(lncRNA)AK126393 in human colorectal cancer cells.Methods The expression of lncRNA AK126393 in normal colon tissue cell lines and colorectal cancer cell lines was detected by quantitative fluorescent PCR(qRT-PCR).The lowest expression cell lines were selected for transfection of lncRNA AK126393 overexpression plasmid and negative control(NC).Cell viability was detected by CCK8 method.Cell cycle and apoptosis were detected by flow cytometry.Protein expressions of Bcl2,Bax,PI 3K,p-PI 3K,Akt,p-Akt and LC3 were detected by Western blotting.Results lncRNA AK126393 was low expressed in colorectal cancer cell lines,with the lowest expression in SW480 cell lines.The relative expression level of lncRNA AK126393 was significantly increased after transfection of SW480 cells with overexpressed plasmid.The ability of cell proliferation decreased significantly,and the level of cell apoptosis increased.Western blotting results showed that the protein expressions of Bcl2,LC3-II,p-PI 3K and p-Akt were significantly increased,the protein expressions of Bax and LC3-I were significantly decreased,and the protein expressions of PI 3K and Akt were not significantly changed.Conclusion lncRNA AK126393 can inhibit the proliferation,promote apoptosis and induce autophagy of colorectal cancer cells by inhibiting PI PI 3K/Akt signaling pathway activation.