敲低LINC00511通过抑制AKT/mTOR信号调控肝癌细胞侵袭迁移

Knockdown of LINC00511 Regulates the Invasion and Migration of Hepatocellular Carcinoma Cells via Inhibiting AKT/mTOR Signaling

目的探索LINC00511对肝癌细胞侵袭以及迁移能力的调节作用以及机制。方法TCGA(the cancer genome atlas)数据库分析LINC00511的组织表达情况;PCR实验检测不同肝癌细胞系中LINC00511的表达;划痕实验分析敲低LINC00511后肝癌细胞迁移能力;Transwell基质胶实验评估细胞侵袭能力;蛋白印记实验评估敲低LINC00511后细胞的AKT/mTOR信号激活情况。结果LINC00511在肝癌组织中高表达(P<0.001);LINC00511在多种肝癌细胞系中高表达(P<0.01);敲低LINC00511后细胞侵袭能力下降,迁移能力下降;敲低LINC00511后AKT/mTOR信号被抑制。结论LINC00511可通过AKT/mTOR信号抑制肝癌细胞侵袭以及迁移。

Objective To explore regulatory effect and the mechanism of LINC00511 on invasion and migration of HCC cells.Methods Tissue expression of LINC00511 was analyzed by TCGA(the cancer genome atlas)database.PCR was used to detect the expression of LINC00511 in different HCC cell lines.The migration ability of HCC cells after LINC00511 knockdown was analyzed by scratch test.The ability of cell invasion was evaluated by Transwell assay.Protein imprinting assay was used to evaluate the activation of the AKT/mTOR signaling after LINC00511 knockdown.Results LINC00511 was highly expressed in hepatocellular carcinoma(P<0.001);LINC00511 was highly expressed in HCC cell lines(P<0.01);after knockdown of LINC00511,the ability of both invasion and migration of HCC cells was decreased.AKT/mTOR signaling was inhibited after LINC00511 knockdown.Conclusion LINC00511 can inhibit the invasion and migration of HCC cells via AKT/mTOR signaling.