JNK1 activated pRb/E2F1 and inhibited p53/p21 signaling pathway is involved in hydroquinone‐induced pathway malignant transformation of TK6 cells by accelerating the cell cycle progression

Author:

Yu Lingxue1ORCID,Qiu Weifeng1,Gao Yuting1,Sun Mingwei12,Chen Lin1,Cui Zheming1,Zhu Delong1,Guo Pu1,Tang Huanwen13ORCID,Luo Hao1

Affiliation:

1. Department of Environmental and Occupational Health, Dongguan Key Laboratory of Environmental Medicine, School of Public Health Guangdong Medical University Dongguan China

2. Faculty of Medicine Macau University of Science and Technology Macao China

3. The First Dongguan Affiliated Hospital Guangdong Medical University Dongguan China

Abstract

AbstractHydroquinone (HQ) is an important metabolites of benzene in the body, and it has been found to result in cellular DNA damage, mutation, cell cycle imbalance, and malignant transformation. The JNK1 signaling pathway plays an important role in DNA damage repair. In this study, we focused on whether the JNK1 signaling pathway is involved in the HQ‐induced cell cycle abnormalities and the underlying mechanism. The results showed that HQ induced abnormal progression of the cell cycle and initiated the JNK1 signaling pathway. We further confirmed that JNK1 suppression decelerated the cell cycle progression through inhibiting pRb/E2F1 signaling pathway and triggering p53/p21 pathway. Therefore, we concluded that JNK1 might be involved in HQ‐induced malignant transformation associated with activating pRb/E2F1 and inhibiting p53/p21 signaling pathway which resulting in accelerating the cell cycle progression.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Guangdong Province

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Management, Monitoring, Policy and Law,Toxicology,General Medicine

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