PARP-1 通过调节 p53 和 p16 参与对 TK6 细胞的氢醌诱导的恶性转化，通过减缓细胞周期实现这一过程。
PARP-1 via regulation of p53 and p16, is involved in the hydroquinone-induced malignant transformation of TK6 cells by decelerating the cell cycle.
机构信息
Department of Environmental and Occupational Health, Dongguan Key Laboratory of Environmental Medicine, School of Public Health, Guangdong Medical University, Dongguan, China.
Department of Environmental and Occupational Health, Dongguan Key Laboratory of Environmental Medicine, School of Public Health, Guangdong Medical University, Dongguan, China.
出版信息
Toxicol In Vitro. 2021 Aug;74:105153. doi: 10.1016/j.tiv.2021.105153. Epub 2021 Mar 24.
Poly(ADP-ribose)polymerase-1 (PARP-1) plays a crucial role in DNA damage repair and could be viewed as both a tumor promoter and tumor-suppressor gene. However, the effects of PARP-1 in hydroquinone-induced malignant transformation of TK6 cells remain to be further elucidated. The present research evaluated the potential mechanism of PARP-1 in hydroquinone-induced malignant transformation of TK6 cells. The results indicated that high PARP-1 inhibited TK6 cells malignant transformation after chronic exposure to HQ. We further confirmed that PARP-1 overexpression blocked cell proliferation, and decelerated cell cycle progression in vitro and in vivo. The immunoblotting analysis indicated that PARP-1 regulated cell cycle progression via p16/Rb and p53. Therefore, we conclude that PARP-1 is involved in HQ-induced malignant transformation associated with increasing p16/Rb and p53 which resulting in decelerating the cell cycle progression.
聚（ADP-核糖）聚合酶-1（PARP-1）在 DNA 损伤修复中发挥着关键作用，它可以被视为既是肿瘤促进基因，也是肿瘤抑制基因。然而，PARP-1 在对苯二酚诱导的 TK6 细胞恶性转化中的作用仍有待进一步阐明。本研究评估了 PARP-1 在对苯二酚诱导的 TK6 细胞恶性转化中的潜在机制。结果表明，高 PARP-1 抑制了慢性 HQ 暴露后 TK6 细胞的恶性转化。我们进一步证实，PARP-1 的过表达在体外和体内均能抑制细胞增殖，并减缓细胞周期进程。免疫印迹分析表明，PARP-1 通过 p16/Rb 和 p53 调控细胞周期进程。因此，我们得出结论，PARP-1 参与了 HQ 诱导的恶性转化，这与增加的 p16/Rb 和 p53 有关，从而减缓了细胞周期进程。
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