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Objective: To explore the function of the miR-18a-5p/CPEB3 axis in regulating the occurrence of hepatocellular carcinoma (HCC). Methods: Differentially expressed miRNAs and mRNAs were acquired by bioinformatics analysis. qRT-PCR was used for miR-18a-5p and CPEB3 mRNA expression detection. Cell functional assays were implemented to examine the biological functions of HCC cells. The binding relationship between miR-18a-5p and CPEB3 was verified by a dual luciferase assay. Results: In HCC, miR-18a-5p was remarkably highly expressed, while CPEB3 was markedly lowly expressed. HCC cell progression was facilitated after cells transfecting miR-18a-5p mimic, whereas silencing miR-18a-5p caused the opposite result. Overexpressing CPEB3 could restore promoting effect of miR-18a-5p on the growth of HCC cells. Conclusion: Oncogene miR-18a-5p accelerates malignant phenotype by suppressing CPEB3. MiR-18a-5p/CPEB3 axis in HCC identified in this study provides a new target for HCC treatment.

Background: As one of the most common cancers in the world, hepatocellular carcinoma (HCC) usually has a poor prognosis. Many HCC patients are usually diagnosed at advanced stages. Therefore, new potential biomarkers for the diagnosis and prognosis of HCC are urgently needed. More and more studies have shown that miR-92a-3p can regulate the occurrence and development of a variety of cancers, but its clinical significance and molecular mechanism in HCC are still elusive. Here, we tried to clarify the regulatory mechanism of miR-92a-3p in HCC. Methods: In this study, we conducted qRT-PCR and revealed that miR-92a-3p was notably upregulated in HCC cells. MTT, flow cytometry, wound healing, Transwell invasion assays and western blot were conducted to uncover that overexpressed miR-92a-3p could boost the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells while inhibiting cell apoptosis. In addition, the proteins associated with PI3K/AKT/mTOR pathway were also detected by western blot. Results: It was suggested that miR-92a-3p could activate the PI3K/AKT/mTOR signaling pathway. Conclusion: These results suggest that miR-92a-3p plays a tumor-promoting role in HCC and may be a potential biomarker for the diagnosis and prognosis of HCC.

The aim of the present study was to investigate the effect of Forkhead box transcription factor M1 (FoxM1)-silencing on the growth, migration and invasion of K1 human papillary thyroid carcinoma (PTC) cells. The effect of FoxM1-small interfering RNA (siRNA) in K1 cells was detected by western blot analysis. FoxM1-siRNA and control siRNA were transfected into K1 cells using Lipofectamine® 2000 (transfection group, T) and the non-meaning sequence group (NM). K1 cells exposed to PBS solution comprised the blank control group (CON). Cell proliferation ability was detected using an MTT assay. Cell migration and invasion was detected by the single cell scratch test and Transwell invasion assay, respectively. Western blot analysis indicated that FoxM1 siRNA downregulated the expression of FoxM1 protein. Cell proliferation, migration and invasion were significantly lower in the T group compared with the NM and CON groups (P<0.05). These results indicated that silencing of FoxM1 expression could block growth, invasion and migration of K1 cells. This study may provide a novel target gene for targeted therapy of PTC.