Fig. 7.

The effects of TrxR1 knock down on proliferation, viability and mechanisms mediating G2/M arrest and apoptosis of HepG2 cells (A) Knock-down of TrxR1 inhibited HepG2 cells proliferation and (B) increased resistance to BS treatment. (C) Immunofluorescent analysis of Trx level upon BS treatment. (D) Gene and (E) protein levels of Trx, Ref-1 and molecules mediating G2/M arrest. (F) Downregulation of NF-κB pathway. Level of (G) mRNA and (H) proteins mediating mitochondria-dependent apoptosis. Data were shown as mean ± std, n ≥ 3 and analyzed with One-way ANOVA. *^{, #}p < 0.05 compared with control or LV-NC-shRNA group.