Abstract
BackgroundLong non-coding RNAs are involved in the pathology of various tumors, including hepatocellular carcinoma. The expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is increased in numerous types of tumors and is involved in tumor cell proliferation, migration, invasion and apoptosis. MALAT1 level was reported to be upregulated in hepatocellular carcinoma tissues, but its roles and the specific molecular mechanisms are still unclear.MethodsThe expression of MALAT1 and miR-142-3p in hepatocellular carcinoma tissues, cell lines and adjacent non-tumor tissues was assessed by Q-PCR. The putative-binding sites between MALAT1 and miR-142-3p were predicted by bioinformatics analysis. The expression of MALAT1 in HepG2 and SMMC-7721 cells was knocked down by transfection with MALAT1 siRNAs. Cell viability was assessed by the Cell Counting Kit-8 (CCK-8) assay after the indicated transfection in HepG2 and SMMC-7721 cells. Cell proliferation was assessed by EdU assay, and cell apoptosis was explored by flow cytometry. The migration and invasion potency of HepG2 and SMMC-7721 cells was assessed by the cell migration assay and matrigel invasion assay. Protein level of vimentin, E-cadherin and SMAD5 were assessed by Western blot.ResultsOverexpressed MALAT1 acts as a competing endogenous RNA sponge for miR-142-3p in hepatocellular carcinoma. The knockdown of MALAT1 inhibited the proliferation, migration, invasion, and epithelial cell-to-mesenchymal transition (EMT), and promoted apoptosis of hepatocellular carcinoma cells via miR-142-3p. MiR-142-3p inhibited cell proliferation, migration, invasion and EMT, and promoted the cell apoptosis by targeting SMAD5 in hepatocellular carcinoma. MALAT1 promoted tumor growth by regulating the expression of miR-142-3p in vivo.ConclusionMALAT1 promoted cell proliferation, migration, and invasion of hepatocellular carcinoma cells by antagonizing miR-142-3p.
Highlights
As the second leading cause of cancer-related deaths worldwide, hepatocellular carcinoma has led to approximately 800,000 deaths and is associated with 850,000 new cases each year [1]
Overexpressed metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) might act as a competing endogenous RNA sponge for miR‐142‐3p in hepatocellular carcinoma Firstly, we assessed the relative expression level of MALAT1 in hepatocellular carcinoma tissues and adjacent non-tumor tissues
By using the bioinformatics databases (Starbase, RNAhybrid) that predict potential Long noncoding RNAs (lncRNAs)-miRNA interactions, we found that miR-142-3p was a putative MALAT1 binding miRNAs (Fig. 1d)
Summary
As the second leading cause of cancer-related deaths worldwide, hepatocellular carcinoma has led to approximately 800,000 deaths and is associated with 850,000 new cases each year [1]. Hepatitis B and C viral infection, intake of alcohol, and exposure to the fungal metabolite aflatoxin B1 are the main risk factors for hepatocellular carcinoma [2, 3]. Primary hepatocellular cancer is a type of heterogeneous tumor in which the tumors metastasizes to hepatocellular tissue from other sites. As the main primary hepatocellular cancer, hepatocellular carcinogenesis is multifactorial process with different susceptibility factors. As the most common primary liver cancer, hepatocellular carcinoma is heterogeneous in nature [6]. The expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is increased in numerous types of tumors and is involved in tumor cell proliferation, migration, invasion and apoptosis. MALAT1 level was reported to be upregulated in hepatocellular carcinoma tissues, but its roles and the specific molecular mechanisms are still unclear
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