Long Non-coding RNA MALAT1 Correlates With The Proliferation Of Hepatocellular Carcinoma Via Sponging MiR-144

OBJECTIVE:Studies have confirmed that long non-coding RNA MALAT1(lncRNA MALAT1)is over-expressing in multiple tumors.MALAT1 can interact with a large number of miRNAs to alter the expression and function of the downstream target genes.Therefore,it can form multiple regulatory networks to induce the occurrence of malignant tumor.However,the underlying mechanism between MALAT1 and miR-144 in hepatocellular carcinoma(HCC)remains to be verified.Our study explored the relationship of MALAT1 and miR-144 in HCC via a series of experiments.It aims to provide a new direction for the effective treatment of HCC.METHODS: Firstly,the expression of MALAT1 and mi R-144 in HCC samples and normal samples was verified through biological databases,and its relationship with the prognosis of HCC patients was analyzed.Meanwhile,the expression levels of MALAT1 and miR-144 was detected by quantitative real?time polymerase chain reaction(RT-qPCR)both in HCC cell lines and normal liver cells.After transfecting si-MALAT1,CCK8 assay and RT-qPCR were used to evaluate the effect of MALAT on the proliferation of HepG2 and Huh7 cells and the expression of miR-144.The relationship of MALAT1 and miR-144 was proved through luciferase reporter assay.Then,the expression level of miR-144 was transformed by miR-144 mimic and miR-144 inhibitor,the proliferation and apoptosis of Huh7 and HepG2 cells was assessed by CCK8 and flow cytometry.The mRNA expression and protein expression levels of the potential target gene MET were detected by RT-qPCR and Western blot.RESULTS: Compared to normal samples,the expression of MALAT1 was up-regulated in HCC tissues.Oppositely,the expression levels of miR-144 was lessened in HCC.And the high expression level of MALAT1 suggested poor prognosis of HCC patients.The proliferation of HCC cells can suppressed by knock-down MALAT1.And si-MALAT1 can augmented the level of miR-144,while the increase of miR-144 in turn induced the apoptosis of HepG2 and Huh7 cells.MALAT1 was the target gene of miR-144.MET was deemed to be a potential target gene of miR-144.The si-MALAT1 inhibited the expression level of MET.However,the West blot and RT-qPCR found the influence of si-MALAT1 on the protein and mRNA expression levels of MET was eliminated by miR-144 inhibitor.CONCLUSION: These results showed MALAT1 has a positive effect on the proliferation of HCC cells,HepG2 and Huh7 cells,which may be achieved by promote the expression of MET through sponging miR-144.The potential regular network between MALAT1,miR-144 and MET may provide a promising therapy for HCC patients.