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. 2020 Aug 25;11(21):6188–6203. doi: 10.7150/jca.45998

Figure 4.

Figure 4

PHLDA1 is a direct target of miR-3682-3p in HCC cells. (A) TargetScan database shows miR-3682-3p putative binding sequence in the 3'-UTR of PHLDA1. The mutant binding site is generated in the complementary site for the seed region of miR-3682-3p. Relation of miR-3682-3p and PHLDA1 in HCC in Starbase database. (B) miR-3682-3p significantly suppressed the luciferase activity that carried wild-type (WT) but not mutant (MT) 3'-UTR of PHLDA1, which led to a notable increase in the luciferase activity of WT 3'-UTR of PHLDA1 in MHCC-97H and Hep3B cell lines. (C) Protein expression of PHLDA1 and Fas, and (D) qRT-PCR analysis of PHLDA1 mRNA expression in MHCC-97H cells with miR-3682-3p inhibitor or NC transfection in MHCC-97H. (E) Protein expression of PHLDA1 and Fas, and (F) qRT-PCR analysis of PHLDA1 mRNA expression in Hep3B cells transfected with miR-3682-3p inhibitor or mimics. (G) WB results of PHLDA1, Fas and P21 relative volume in nodule tissues. Bar figures indicated the statistics. *P<0.05, **P<0.01. n = 3 independent experiments.