p16 loss facilitate hydroquinone-induced malignant transformation of TK6 cells through promoting cell proliferation and accelerating the cell cycle progression
p16 loss facilitate hydroquinone-induced malignant transformation of TK6 cells through promoting cell proliferation and accelerating the cell cycle progression
复制标题
p16 缺失促进氢醌通过促进细胞增殖和加速细胞周期进程诱导 TK6 细胞恶性转化
DOI：
10.1002/tox.23155
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发表时间：
2021-05-01
影响因子：
4.5
通讯作者：
Tang, Huanwen
中科院分区：
文献类型：
--
作者：
Luo, Hao;Zhai, Lu;Tang, Huanwen
p16（INK4A）是一个多功能基因，包括调控细胞周期、凋亡、衰老和肿瘤发展。然而，p16在对苯二酚诱导的TK6细胞恶性转化中的作用尚不清楚。本研究旨在探讨p16缺失是否促进了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的TK6细胞恶性转化中受到抑制。我们进一步证实p16缺失刺激了细胞增殖，加速了细胞周期的进展。免疫印迹分析显示p16通过Rb和p53调控细胞周期进程。因此，我们得出结论，p16参与了红旗诱导的恶性转化，并与抑制Rb和p53相关，从而加速细胞周期进程。
The p16(INK4A) 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.