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Background: Accumulating evidence suggests an antineoplastic role of MicroRNA-34a ( miR-34a ) in human cancer. However, its precise biological functions stay largely elusive. Purpose: Our study was aimed to investigate the impact of miR-34a on hepatocellular carcinoma (HCC) and its underlying apoptosis related mechanisms in vitro, as well as the association of miR-34a ,  E2F1  and  E2F3  expression with patient survival of HCC using publicly accessed datasets. Methods: The HBV-expressing Hep3B and SNU-449 cell lines with or without enforced expression of miR-34a were in vitro cultured for cell proliferation, colony formation, wound healing, cell invasion, and 3D spheroid formation. Quantitative reverse transcription PCR (RT-qPCR) was performed for  E2F1, E2F3  expression. Caspase-3 (CASP3) activity was determined using a CaspACE TM  Assay System. Kaplan-Meier survival curves were used to analyze the associations of miR-34a,  E2F1  and  E2F3  expression and overall survival in HCC. Meta-analysis was performed to examine the differential expression of  E2F1  and  E2F3  between primary HCC vs normal tissues. Results:  The results in vitro showed that enforced miR-34a expression significantly inhibited cell proliferation, migration, and invasion of both Hep3B and SNU-449. RT-qPCR results demonstrated that miR-34a could significantly suppress  E2F1  and  E2F3  expression, particularly in SNU-449. CASP3 activity in both Hep3B and SNU-449 increased in miR-34a treatment group. Overexpressed  E2F1  and  E2F3  were observed in primary HCC vs normal tissues. Survival analyses showed that HCC patients with either high miR-34a , or low  E2F1 , or low  E2F3  expression had better survival than their opposite counterparts, respectively. Conclusion : Our study suggested that miR-34a can modulate the expression of  E2F1, E2F3 , and CASP3 activity, thereby repressing tumor aggressiveness and expediting apoptosis in liver cancer cells.

cancer management and research

&lt;p&gt;MicroRNA-34a suppresses aggressiveness of hepatocellular carcinoma by modulating &lt;em&gt;E2F1&lt;/em&gt;, &lt;em&gt;E2F3&lt;/em&gt;, and Caspase-3&lt;/p&gt;