MALAT1 Mediated LTBP3 Expression Promotes HepG2 Cell Proliferation and Migration by Activating Akt Signaling Pathway

The metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and latent TGF-beta binding protein 3 (LTBP3) gene was identified to be upregulated in cancer cells. We performed this study to investigate whether MALAT1-mediated LTBP3 expression and cellular behavior were associated with Akt signaling pathway in HepG2 cells. HepG2 cells were transfected with siRNAs against MALAT1 and LTBP3, and pcDNA plasmid encoding LTBP3 protein. L02 cell line was employed as normal control. Cell viability, migration, and p-Akt protein expression were detected using MTT, wound healing (scratch wound), real-time PCR and western blot analysis, respectively. The effect of MALAT1 expression on cellular behaviors and activation of LTBP3 and Akt signaling pathway would be discussed. In comparison with L02 cells, the overexpression of MALAT1 and LTBP3 was detected in HepG2 cells. Cell proliferation and migration was significantly inhibited in HepG2 cells transfected with si-MALAT1 and si-LTBP3 compared with control. On the contrary, transfection of pc-LTBP3 plasmid enhanced HepG2 cells viability and migration. Moreover, a positive correlation between LTBP3 and Akt phosphorylation was observed in HepG2 cells. The expression of MALAT1 and LTBP3 were correlated with HepG2 cells proliferation and migration through Akt signaling pathway.