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

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

  • Chem Res Toxicol. 2024 May 21. doi: 10.1021/acs.chemrestox.4c00025.
Wan-Ting Ou 1 Qiu-Xian Wan 1 Yi-Bo Wu 1 Xuan Sun 1 Yan-Li Li 1 Dan Tang 1 Jian Zhang 1 Sheng-Sheng Li 1 Nuo-Yan Wang 1 Zhuo-Lin Liu 1 Jian-Jun Wu 1 2
Affiliations

Affiliations

  • 1 School of Public Health, Guangzhou Medical University, Guangzhou 511436, P. R. China.
  • 2 State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, P. R. China.
Abstract

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.

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