Fig. 4

Cx32 exerts an anti-apoptotic effect on HepG2 cells in a GJ-independent manner. a. When GJ function was inhibited by pretreatment with 2-APB (50 μm, 2 h), knockdown of Cx32 promoted the SN-induced increase in the levels of cleaved-caspase3 and cleaved-PRAR in HepG2 cells, as revealed by western blot analysis (n = 3). ^**, P < 0.01; ^##, P < 0.01. b. Silencing the expression of Cx32 promoted SN-induced apoptosis in HepG2 cells when GJ function was inhibited by 2-APB, as assessed by flow cytometry (n = 3). ^##, P < 0.01 versus NC; ^**, P < 0.01 versus NC + 2-APB + SN. c. When GJs were physically eliminated by low-density culture conditions, Cx32 silencing enhanced the SN-induced increase in the levels of cleaved-caspase3 and cleaved-PARP in HepG2 cells, as revealed by western blot analysis (n = 3). ^**, P < 0.01; ^##, P < 0.01. d. Cx32 silencing facilitated SN-induced apoptosis in HepG2 cells in low-density culture, as assessed by flow cytometry (n = 3). ^**, P < 0.01 versus NC + SN