Alterations of DNA methylation and mRNA levels of CYP1A1 , GSTP1, and GSTM1 in human bronchial epithelial cells induced by benzo[a]pyrene

• Published in: Toxicology and industrial health Vol. 38; no. 3; p. 127
• Main Authors: Liu, Aixiang, Li, Xin, Hao, Zhongsuo, Cao, Jingjing, Li, Huan, Sun, Min, Zhang, Zhihong, Liang, Ruifeng, Zhang, Hongmei
• Format: Journal Article
• Language: English
• Published: England 01.03.2022
• Subjects: Benzo(a)pyrene - toxicity; Cytochrome P-450 CYP1A1 - genetics; Cytochrome P-450 CYP1A1 - metabolism; DNA Adducts; DNA Methylation; Epithelial Cells - metabolism; Genotype; Glutathione S-Transferase pi - genetics; Glutathione Transferase - genetics; Glutathione Transferase - metabolism; Humans; Polymorphism, Genetic; RNA, Messenger - genetics; DNA methylation; Benzo[a]pyrene; mRNA; cell proliferation; 16HBEs
• ISSN: 1477-0393
• DOI: 10.1177/07482337211069233

Benzo[a]pyrene (B[a]P) is a known human carcinogen and plays a major function in the initiation of lung cancer at its first proximity. However, the underlying molecular mechanisms are less well understood. In this study, we investigated the impact of B[a]P treatment on the DNA methylation and mRNA levels of , and in human bronchial epithelial cells (16HBEs), and provide scientific evidence for the mechanism study on the carcinogenesis of B[a]P. We treated 16HBEs with DMSO or concentrations of B[a]P at 1, 2, and 5 mmol/L for 24 h, observed the morphological changes, determined the cell viability, DNA methylation, and mRNA levels of , and . Compared to the DMSO controls, B[a]P treatment had significantly increased the neoplastic cell number and cell viability in 16HBEs at all three doses (1, 2, and 5 mmol/L), and had significantly reduced the and DNA promoter methylation levels. Following B[a]P treatment, the promoter methylation level in 16HBEs was profoundly reduced at low dose group compared to the DMSO controls, yet it was significantly increased at both middle and high dose groups. The levels of , and were significantly decreased in 16HBEs following B[a]P treatment at all three doses. The findings demonstrate that B[a]P promoted cell proliferation in 16HBEs, which was possibly related to the altered DNA methylations and the inhibited mRNA levels in , and .