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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).<br /><br /> 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.<br /><br />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.<br /><br /> CDKN2C exerts critical functions during the progression of hepatocellular carcinoma (HCC). [https://www.selleckchem.com/products/OSI-906.html Linsitinib concentration] 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.<br /><br /> 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.<br /><br /> There were five miRNAs predicted to bind to CDKN2C and among them, miRNA-22-3p and miRNA-182-5p were markedly downregulated in LIHC tissues. In Huh7 and Hep3B cells, miRNA-22-3p negatively regulated CDKN2C level, while transfection of miRNA-182-5p mimic or inhibitor did not influence CDKN2C expression. MiRNA-22-3p was closely linked to poor prognosis of HCC patients. Subsequently, dual-luciferase reporter gene assay verified the binding between miRNA-22-3p and CDKN2C.<br /><br /> Knockdown of miRNA-22-3p suppressed proliferative ability and arrested cell cycle progression, which were reversed by overexpression of CDKN2C. MiRNA-22-3p suppresses proliferative ability and arrests cell cycle progression in HCC through targeting CDKN2C.<br /><br />Knockdown of miRNA-22-3p suppressed proliferative ability and arrested cell cycle progression, which were reversed by overexpression of CDKN2C. MiRNA-22-3p suppresses proliferative ability and arrests cell cycle progression in HCC through targeting CDKN2C.<br /><br /> To investigate whether RBM6 can serve as a suppressor gene in hepatocellular carcinoma (HCC) and affect its progression.<br /><br /> QPCR and Western blot were carried out to measure RBM6 expression in tissue samples collected from HCC patients with different tumor sizes or in different stages. The relationship between overall survival (OS) and RBM6 expression in patients with HCC was analyzed using Kaplan-Meier survival method. Meanwhile, the effects of different factors on HCC progression were evaluated through Cox regression analysis. After over-expression of RBM6 in HepG2 and HB611 cells, the cell viability, cell migration and invasion abilities and apoptosis rate were assessed by cell counting kit-8 (CCK-8), transwell assay, and flow cytometry analysis, respectively.<br /><br /> RBM6 expression, markedly down-regulated in HCC tissues, showed a great relevance to tumor size, TNM stage, and histological grade, and the survival rate of patients in high RBM6 expression group was higher than those in low RBM6 expression group. Besides, Cox regression analysis revealed that RBM6 expression, tumor size, TNM stage and histological grade were four independent factors affecting the OS of HCC patients. Moreover, in vitro cell experiments demonstrated that overexpression of RBM6 significantly attenuated the cell viability as well as the invasive ability while enhanced cell apoptosis.<br /><br /> The low expression of RBM6 contributes to the improvement of the survival of patients with HCC. Therefore, RBM6 can serve as a tumor-suppressing gene to repress cell proliferation, migration and invasion and promote cell apoptosis, thereby affecting the progression of HCC.<br /><br />The low expression of RBM6 contributes to the improvement of the survival of patients with HCC. Therefore, RBM6 can serve as a tumor-suppressing gene to repress cell proliferation, migration and invasion and promote cell apoptosis, thereby affecting the progression of HCC.<br /><br /> The purpose of this study was to elucidate the role of Baicalein in accelerating invasiveness and inducing apoptosis of glioma cells through the phosphatidilinositol 3-kinase/protein kinase B (PI3K/Akt) pathway.<br /><br /> U251 glioma cells were treated with different doses of Baicalein (10, 20 or 40 μM) for different time periods (12, 24, 36 or 48 h). Changes in viability, clonality, cell cycle distribution and apoptosis in Baicalein-treated U251 cells were assessed. Meanwhile, relative levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 in U251 cells were detected. Western blot was conducted to examine protein levels of p-Akt and Akt in Baicalein-treated U251 cells.<br /><br /> Baicalein treatment attenuated dose-dependently and time-dependently the viability and clonality in U251 cells. It induced cell cycle arrest in G0/G1 phase and cell apoptosis of U251 cells. After Baicalein treatment, the relative levels of MMP-2 and MMP-9 were dose-dependently downregulated. Baicalein treatment activated the PI3K/Akt pathway. Notably, inhibitory effects of Baicalein treatment on MMP levels and invasiveness in glioma were blocked by the application of LY294002 (PI3K/Akt inhibitor), and stimulated by the application of IGF-1 (PI3K/Akt activator).<br /><br /> Baicalein treatment is able to suppress invasiveness and induce apoptosis of glioma cells through inactivating the PI3K/Akt pathway.<br /><br />Baicalein treatment is able to suppress invasiveness and induce apoptosis of glioma cells through inactivating the PI3K/Akt pathway.