The Upregulation Of Microrna-223 Promoted The Apoptosis Of Liver Cancer Cells Via Tlr4

Liver cancer (LC) is the third largest contributor to mortality related to malignancies worldwide. The study was directed toward exploring the effects of miR-223 on LC proliferation and apoptosis. Dual luciferase reporter assay (DLRA) was carried out to verify the direct relationship of TLR4 mRNA 3 ' -UTR and miR-223-3p. HepG2 cells subsequently were transfected with miR-223 mimics. MTT assay and flow cytometric assay were carried out to evaluate proliferation and cell death, respectively. Toll-like receptor 4 (TLR4) transcription and translation were examined via qRT-PCR and western blotting, respectively. We observed that the miR-223 expression in LC tissues was inhibited, accompanied by reinforced TLR4 expression. Excessive miR-223 expression noticeably inhibited cell growth and promoted apoptosis in HepG2 and Bel-7402 HCC cell lines. Additionally, knockdown of TLR4 expression could suppress cell growth and promote apoptosis in HepG2 and Bel-7402 HCC cell lines. Moreover, TLR4 expression was suppressed via miR-223 transfection. T DLRA verified that miR-223 directly targeted TLR4. TLR4 over-expression canceled the effects of miR-223 on LC proliferation and apoptosis. Collectively, our findings suggest that miR-223 is an inhibitor of malignancy and participates in the inhibition of malignancy generation and reinforcement of LC cell death by targeting TLR4.