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https://www.selleckchem.com/products/dl-ap5-2-apv.html The proliferation and migration in HCC cells were inhibited by overexpression of miR-497, which were enhanced after transfection with miR-497 inhibitor. miR-497 had an effect on VEGF-B levels and there was a regulatory relationship between them. miR-497 was able to target VEGF-B and downregulate the receptor of VEGF-B (FLT-1). miR-497 was lowly expressed in HCC tissues, and its overexpression inhibited invasion and metastasis in HCC cells by suppressing VEGF-B levels. MiR-497 and its target gene VEGF-B are closely associated with the biological function and may serve as prognostic factors of MVI in patients with HCC. miR-497 was lowly expressed in HCC tissues, and its overexpression inhibited invasion and metastasis in HCC cells by suppressing VEGF-B levels. MiR-497 and its target gene VEGF-B are closely associated with the biological function and may serve as prognostic factors of MVI in patients with HCC. CDKN2C exerts critical functions during the progression of hepatocellular carcinoma (HCC). Its dysfunction is closely linked to poor prognosis of HCC. This study aimed to uncover the underlying mechanism of CDKN2C in affecting the prognosis of HCC. Potential miRNAs that could regulate CDKN2c were predicted by bioinformatics, and their differential levels in HCC and normal liver tissues were detected. CDKN2C level in Huh7 and Hep3B cells influenced by the two candidate microRNAs, miRNA-22-3p and miRNA-182-5p, were examined. Correlation between miRNA-22-3p and CDKN2C in HCC was analyzed on LinkedOmics, and further confirmed by Pearson correlation test and dual-luciferase reporter gene assay. Thereafter, the prognostic potential of miRNA-22-3p in HCC was evaluated by Kaplan-Meier method. Furthermore, the regulatory effects of miRNA-22-3p/CDKN2C axis on proliferative ability and cell cycle progression of HCC were assessed. There were five miRNAs predicted to bind to CDKN2C and among them, miRNA-22-3p and miRNA-18

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