Activation of alternative apoptosis pathways in HepG2 cells after caspase arrest

Aims: Actinomycin D-sensitized HepG2 cells are highly susceptible to induction of apoptosis via stimulation of death receptors (TNF-R1, CD95 and TRAIL receptor) [1]. We and others showed that the pan-caspase inhibitor zVAD-fmk conferred complete protection of HepG2 cells against apoptosis induced by TNFα or agonistic anti-CD95 antibody [2]. Here we provide evidence that in presence of zVAD-fmk HepG2 cells can switch to caspase-independent apoptotic signaling pathways. Results: HepG2 cells were incubated with different apoptosis-inducing stimuli in presence or absence of various inhibitors. Apoptosis was characte…