Long Noncoding RNA PSMB8-AS1 Mediates the Tobacco-Carcinogen-Induced Transformation of a Human Bronchial Epithelial Cell Line by Regulating Cell Cycle

• Published in: Chemical research in toxicology 2024-06, Vol.37 (6), p.957-967
• Main Authors: Ou, Wan-Ting, Wan, Qiu-Xian, Wu, Yi-Bo, Sun, Xuan, Li, Yan-Li, Tang, Dan, Zhang, Jian, Li, Sheng-Sheng, Wang, Nuo-Yan, Liu, Zhuo-Lin, Wu, Jian-Jun
• Format: Article
• Language: English
• Subjects: Bronchi - cytology; Bronchi - drug effects; Bronchi - pathology; Carcinogens - toxicity; Cell Cycle - drug effects; Cell Line; Cell Movement - drug effects; Cell Proliferation - drug effects; Epithelial Cells - drug effects; Epithelial Cells - metabolism; Epithelial Cells - pathology; Humans; Nicotiana - chemistry; Nitrosamines - toxicity; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism
• ISSN: 0893-228X; 1520-5010; 1520-5010
• DOI: 10.1021/acs.chemrestox.4c00025

Lung cancer is the main cause of cancer deaths around the world. Nitrosamine 4-(methyl nitrosamine)-1-(3-pyridyl)-1-butanone (NNK) is a tobacco-specific carcinogen of lung cancer. Abundant evidence implicates long noncoding RNAs (lncRNAs) in tumorigenesis. Yet, the effects and mechanisms of lncRNAs in NNK-induced carcinogenesis are still unclear. In this study, we discovered that NNK-induced transformed Beas-2B cells (Beas-2B-NNK) showed increased cell migration and proliferation while decreasing rates of apoptosis. RNA sequencing and differentially expressed lncRNAs analyses showed that lncRNA PSMB8-AS1 was obviously upregulated. Interestingly, silencing the lncRNA PSMB8-AS1 in Beas-2B-NNK cells reduced cell proliferation and migration and produced cell cycle arrest in the G2/M phase along with a decrease in CDK1 expression. Conclusively, our results demonstrate that lncRNA PSMB8-AS1 could promote the malignant characteristics of Beas-2B-NNK cells by regulating CDK1 and affecting the cell cycle, suggesting that it may supply a new prospective epigenetic mechanism for lung cancer.