NDLI: Nuclear respiratory factor 1 overexpression attenuates anti-benzopyrene7,8-diol-9,10-epoxide-induced S-phase arrest of bronchial epithelial cells.

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Nuclear respiratory factor 1 overexpression attenuates anti-benzopyrene7,8-diol-9,10-epoxide-induced S-phase arrest of bronchial epithelial cells.

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Nuclear respiratory factor 1 overexpression attenuates anti-benzopyrene7,8-diol-9,10-epoxide-induced S-phase arrest of bronchial epithelial cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wu, Jing Wang, Yaning Zhang, Lijuan Li, Jue Wo, Da
Description	Author Affiliation: Wu J ( Division of Preventive Medicine, Tongji University School of Medicine, Shanghai 200092, P.R. China.); Wang Y ( Division of Preventive Medicine, Tongji University School of Medicine, Shanghai 200092, P.R. China.); Wo D ( Division of Preventive Medicine, Tongji University School of Medicine, Shanghai 200092, P.R. China.); Zhang L ( Division of Preventive Medicine, Tongji University School of Medicine, Shanghai 200092, P.R. China.); Li J ( Division of Preventive Medicine, Tongji University School of Medicine, Shanghai 200092, P.R. China.)
Abstract	Nuclear respiratory factor 1 (NRF-1) has important roles in the regulation of several key metabolic genes required for cellular growth and respiration. A previous study by our group indicated that NRF1 is involved in mitochondrial dysfunction induced by the environmental pollutant benzo[a]pyrene in the 16HBE human bronchial epithelial cell line. In the present study, it was observed that its genotoxic metabolite, antibenzopyrene7,8diol9,10epoxide (BPDE), triggered cell cycle arrest in Sphase in 16HBE cells by activating ataxia-telangiectasia (ATM)/checkpoint kinase (Chk)2 and ATM and Rad3 related (ATR)/Chk1 signaling pathways. NRF1 expression was suppressed by BPDE after treatment for 6 h. Flow cytometric analysis revealed that NRF1 overexpression attenuated cell cycle arrest in Sphase induced by BPDE. In line with this result, DNAdamage checkpoints were activated following NRF1 overexpression, as demonstrated by increased phosphorylation of ATM, Chk2 and Î³H2AX, but not ATR and Chk1, according to western blot analysis. It was therefore indicated that NRF1 overexpression attenuated BPDEinduced Sphase arrest via the ATM/Chk2 signaling pathway.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	13
Language	English
Publisher	Spandidos Publications
Publisher Date	2016-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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