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. 2021 Jun 1;22(11):6001. doi: 10.3390/ijms22116001

Figure 6.

Figure 6

Overexpression of MIR29A-3p in HepG2 cells might induce apoptosis signaling and inhibits wound healing performance, and viability. HepG2 cells treated with transfection reagent as a control (Ctrl), MIRs negative sequence (NC), or MIR29A-3p mimic (mimic) for 24 h, followed by further assays. The activity of apoptosis signaling was examined by probing the cleaved (37 and 35 kDa)/non-cleaved (46 kDa) caspase-9 (CASP9) (A), cleaved caspase-3 (CASP3) (B), and cleaved poly (ADP-ribose) polymerase (PARP) (C). GAPDH as loading control. The ratio of cleaved/non-cleaved CASP9, and the GAPDH-normalized cleaved CASP3 and cleaved PARP were analyzed for the densitometric quantification. (D) Representative image at 0 h and 120 h of wound healing assay. (E) Quantification histogram of the changed area percentage (∆Area%) of the scratched ditch determined by the migrated cells. (F) Cell viability detected by WST-1-based OD450 signal. * p < 0.05, ** p < 0.01, *** p < 0.001 between indicated groups.