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.

中文翻译：

---

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 ^INK4A是一种多功能基因，包括调节细胞周期、细胞凋亡、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仍不清楚。本研究旨在探讨 p16 缺失是否会促进 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，与抑制 Rb 和 p53 相关，从而加速细胞周期进程。