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p16 缺失通过促进细胞增殖和加速细胞周期进程促进对苯二酚诱导的 TK6 细胞恶性转化。

p16 loss facilitate hydroquinone-induced malignant transformation of TK6 cells through promoting cell proliferation and accelerating the cell cycle progression.

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.

出版信息

Environ Toxicol. 2021 Aug;36(8):1591-1599. doi: 10.1002/tox.23155. Epub 2021 May 1.

DOI:10.1002/tox.23155
PMID:33932074
Abstract

The p16 is a multifunction gene that includes regulation of the cell cycle, apoptosis, senescence and tumor development. However, the effects of p16 in hydroquinone-induced malignant transformation of TK6 cells remain unclear. The present study aimed to explore whether p16 loss facilitate malignant transformation in TK6 cells. The results demonstrated that p16/Rb signal pathway was suppressed in hydroquinone-induced malignant transformation of TK6 cells. We further confirmed that p16 loss stimulated cell proliferation, and accelerated cell cycle progression in vitro and in vivo. The immunoblotting analysis indicated that p16 regulated cell cycle progression via Rb and p53. Therefore, we conclude that p16 is involved in HQ-induced malignant transformation associated with suppressing Rb and p53 which resulting in accelerating the cell cycle progression.

摘要

p16 是一个多功能基因,包括细胞周期调控、细胞凋亡、衰老和肿瘤发生。然而,p16 在对苯二酚诱导 TK6 细胞恶性转化中的作用尚不清楚。本研究旨在探讨 p16 缺失是否促进 TK6 细胞的恶性转化。结果表明,p16/Rb 信号通路在对苯二酚诱导 TK6 细胞恶性转化中受到抑制。我们进一步证实,p16 缺失可刺激细胞增殖,并在体外和体内加速细胞周期进程。免疫印迹分析表明,p16 通过 Rb 和 p53 调节细胞周期进程。因此,我们得出结论,p16 参与 HQ 诱导的恶性转化,抑制 Rb 和 p53,从而加速细胞周期进程。

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