miR-103通过抑制LATS2促进肝细胞肝癌侵袭转移的机制

MiRNA-103 promotes tumor growth and metastasis in hepatocellular carcinoma through LATS2

目的研究原发性肝癌中miR-103的表达及对肝癌细胞系转移能力的影响。方法 RT-PCR检测miR-103在肝癌组织及肝癌源性细胞系中的表达。分别转染miR-103 mimic至L02细胞、转染miR-103抑制剂至HepG2细胞,CCK8法检测miR-103对细胞增殖的影响,TUNEL法检测miR-103对细胞凋亡的影响,Transwell实验检测miR-103对肿瘤细胞侵袭和转移的影响。生物信息学分析miR-103的靶基因,western blot验证靶基因表达与rmiR-103的相关性。结果 miR-103在肝癌标本和肝癌源性细胞系中表达上调,miR-103可以促进细胞增殖,抑制细胞凋亡,Transwell实验结果表明miR-103增加细胞侵袭和转移能力。生物信息学分析表明拉特抑癌基因同源分子2(LA,TS2)为miR-103的潜在靶基因。miR-103的表达与LATS2呈负相关。结论以上数据证明miR-103通过抑制LA,TS2促进肝细胞肝癌侵袭转移,miR-103/LA,TS2失调有可能成为治疗肝癌的新靶点。

Objective To investigate miRNA-103 （miR-103） expression and its roles in human hepatocellular carcinoma （HCC）. Methods The expression of miR-103 in HCC samples and HCC derived cell lines was detected using real time RT-PCR. miR - 103 mimic was transfected into IO2 cells, while miR - 103 inhibitor was transfeeted into HepG2 cells, respectively. Cell prolifer- ation was detected by CCK8 kit. Apoptosis was detected using TUNEL staining. The cell invasion and metastasis were detected using Transewell assay. The target genes of miR-103 was screened using bioinformatics analysis and confirmed by western blot. Results The miR - 103 expression was up regulated in HCC specimens and cell lines, miR - 103 can promote cell proliferation, inhibit the ap- optosis, miR - 103 increase invasion and metastasis. Bioinformatics analysis showed that tumor suppressor gene 2 （EATS2） as the po- tential target genes of miR - 103. The expression of miR - 103 and negatively correlated with LATS2. Conclusion The above data proved that miR - 103 promote the invasion and metastasis of HCC by inhibiting LATS2, miR - 103/LATS2 disfunction may be poten- tial targets for the treatment of HCC.