PARP-1 via regulation of p53 and p16, is involved in the hydroquinone-induced malignant transformation of TK6 cells by decelerating the cell cycle. (August 2021)

• Record Type: Journal Article
• Authors: Zhai, Lu; Liang, Hairong; Du, Jinlin; Sun, Mingwei; Qiu, Weifeng; Tang, Huanwen; Luo, Hao
• Is Part Of: Toxicology in vitro. Volume 74(2021)
• Publication Date: 2021-08
• Subjects: Hydroquinone -- PARP-1 -- Malignant transformation -- Cell cycle -- p53 -- p16; Toxicity testing -- In vitro -- Periodicals; Toxicology -- Periodicals; 615.9
• DOI: 10.1016/j.tiv.2021.105153
• Languages: English
• ISSNs: 0887-2333

Abstract

Abstract: 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. Highlights: Hydroquinone (HQ) is a carcinogen, which affects proliferation and cell cycle in lymphoma cells. PARP-1 plays a crucial role in DNA damage repair and could be viewed as both a tumor promoter and tumor-suppressor gene. High PARP-1 inhibited TK6 cells malignant transformation after chronic exposure to HQ via decelerating the cell cycle. PARP-1 via regulating p53 and p16, is involved in HQ-induced malignant transformation.