Di-san junyi daxue xuebao (Jul 2021)
MiR-3934-5p promotes proliferation of hepatocellular carcinoma cells by targeting LACTB
Abstract
Objective To explore the expression, clinical significance and molecular mechanism of miR-3934-5p in hepatocellular carcinoma (HCC). Methods HCC tissues and adjacent normal tissues were collected from 53 HCC patients diagnosed in our hospital from September 2013 to August 2014. Real-time quantitative PCR (RT-qPCR) was performed to detect the level of miR-3934-5p in the above tissues and human liver cell line L02 and HCC cell lines. The Cancer Genome Atlas (TCGA) database was used to analyze the expression of miR-3934-5p in normal liver tissues and HCC tissues; Chi-square test with Kaplan-Meier survival curve were applied to analyze the correlation of miR-3934-5p and clinicopathological characteristics and survival prognosis; RT-qPCR and Western blotting were adopted to detect transfection efficiency; CCK-8 assay, colony formation assay and EdU assay were employed respectively to evaluate the activity and proliferation of HCCLM3 cells; Spearman correlation analysis was applied to study the correlation between LACTB mRNA and miR-3934-5p expression in HCC tissues; TargetScan database was used to predict the downstream target genes of miR-3934-5p, and the prediction results was verified by luciferase reporter assay. Results MiR-3934-5p was highly expressed in the liver cancer tissues and cells (P < 0.05), and its high expression was significantly correlated with tumor size (P=0.040), tumor multiplicity (P=0.013), vascular invasion (P=0.006), and TNM stage (P=0.017); Compared to the low miR-3934-5p expression group, the HCC patients with high expression had poorer survival prognosis. CCK-8 assay, colony formation assay and EdU assay confirmed that knocking down miR-3934-5p notably inhibited the proliferation of HCCLM3 cells (P < 0.05). LACTB had been proved to be the direct target of miR-3934-5p, and mediated the biological effect of miR-3934-5p on HCC cells. Conclusion MiR-3934-5p promotes the proliferation of HCC cells by targeting tumor suppressor gene LACTB.
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