4.7 Article

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

Journal

ENVIRONMENTAL TOXICOLOGY
Volume 36, Issue 8, Pages 1591-1599

Publisher

WILEY
DOI: 10.1002/tox.23155

Keywords

cell cycle; hydroquinone; malignant transformation; p16

Funding

  1. Dongguan Key Laboratory of Environmental Medicine
  2. Guangdong Medical University [GDMU2018099]
  3. Guangdong Provincial Natural Science Foundation [2018A030313580]
  4. National Natural Science Foundation of China [81803278]
  5. GuangdongProvincial major scientific research projects of ordinary universities [2017KZDXM041]
  6. Provincial and municipal joint projects [4SG18056G, 4SG18102G, 4SG18004G, 4SG17043]

Ask authors/readers for more resources

The study revealed that the p16/Rb signal pathway is suppressed in hydroquinone-induced malignant transformation of TK6 cells, resulting in enhanced cell proliferation and accelerated cell cycle progression. It was further confirmed that p16 regulates cell cycle progression via Rb and p53, indicating its involvement in hydroquinone-induced malignant transformation.
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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available