Poly(ADP-ribose)polymerase-1 affects hydroquinone-induced aberrant cell cycle and apoptosis through activation of p16/pRb signaling pathway in TK6 cells

• Published in: Ecotoxicology and environmental safety 2022-03, Vol.232, p.113259-113259, Article 113259
• Main Authors: Luo, Hao, Chen, Lin, Cui, Zheming, Du, Jinlin, Yang, Hui, Qiu, Weifeng, Zhai, Lu, Liang, Hairong, Tang, Huanwen
• Format: Article
• Language: English
• Subjects: Adenosine Diphosphate - pharmacology; Apoptosis; Cell Cycle; Hydroquinone; Hydroquinones - toxicity; P16; PARP-1; Poly (ADP-Ribose) Polymerase-1 - genetics; Poly (ADP-Ribose) Polymerase-1 - metabolism; Ribose - pharmacology; Signal Transduction
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2022.113259

Hydroquinone (HQ), a key metabolite of benzene, affects cell cycle and apoptosis. Poly (ADP-ribose) polymerase-1 (PARP-1) plays an important role in DNA damage repair. To explore whether PARP-1 is involved in HQ-induced cell cycle and apoptosis, we assessed the effect of PARP-1 suppression and overexpression on induction of cell cycle and apoptosis analyzed by flow cytometry analysis. We observed that HQ induced aberrant cell cycle progression and apoptosis. We further confirmed that PARP-1 suppression accelerated the cell cycle progression and inhibited cell apoptosis via inhibiting p16/pRb signal pathway after acute HQ exposure, while overexpression of PARP-1 displayed the opposite results. Therefore, we concluded that HQ-induced cell cycle and apoptosis were regulated by PARP-1 through activation of p16/pRb signaling pathway. [Display omitted] •HQ is a carcinogen, which affect cell cycle and apoptosis in lymphoma cells.•PARP-1 plays an important role in DNA damage repair.•PARP-1 is involved in HQ-induced cell cycle and apoptosis through regulating p16/pRb signaling pathway.•JNK1 signal pathway is not involved in the interaction of PARP-1 with p16 after exposure to HQ.