Hydroquinone induces TK6 cell growth arrest and apoptosis through PARP‐1/p53 regulatory pathway

Hydroquinone (HQ), one of the most important metabolites derived from benzene, induces cell cycle arrest and apoptosis. Poly(ADP‐ribose) polymerase‐1 (PARP‐1) participates in various biological processes, including DNA repair and cell cycle regulation. To explore whether PARP‐1 regulatory pathway mediated HQ‐induced cell cycle arrest and apoptosis, we assessed the effect of PARP‐1 suppression on induction of apoptosis analyzed by FACSCalibur flow cytometer in PARP‐1 deficientTK6 cells (TK6‐shPARP‐1). We observed an increase in the fraction of cells in G1 phase by 7.6% and increased apoptosis by 4.5% in PARP‐1‐deficient TK6 cells (TK6‐shPARP‐1) compared to those negative control cells (TK6‐shNC cells) in response to HQ treatment. Furthermore, HQ might activate the extrinsic pathways of apoptosis via up‐regulation of Fas expression, followed by caspase‐3 activation, apoptotic body, and sub G1 accumulation. Enhanced p53 expression was observed in TK6‐shPARP‐1 cells than in TK6‐shNC cells after HQ treatment. In contrast, Fas expression was lower in TK6‐shPARP‐1 cells than in TK6‐shNC cells. Therefore, we conclude that HQ may activate apoptotic signals via Fas up‐regulation and p53‐mediated apoptosis in TK6‐shNC cells. The reduction of PARP‐1 expression further intensified up‐regulation of p53 in TK6‐shPARP‐1 cells, resulting in an increased G1→S phase cell arrest and apoptosis in TK6‐shPARP‐1 cells compared to TK6‐shNC cells.