Downregulation of the phosphatase PHLPP1 contributes to NNK-induced malignant transformation of human bronchial epithelial cells (HBECs).

ABSTRACT: Cigarette smoking (CS) is one of the greatest health concerns, which can cause lung cancer. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a tobacco-specific nitrosamine, has been well-documented for its carcinogenic activity in both epidemiological and laboratory studies. PH domain leucine-rich repeat protein phosphatase 1 (PHLPP1) and phosphatase and tensin homolog (PTEN) are two well-known phosphatase tumor suppressors that have been reported to be downregulated in human lung cancer tissues. However, the effect of NNK exposure on the expression of PHLPP1 and PTEN is unknown, and such effects may be early events leading to lung carcinogenesis. We explored this question in current studies and found that exposure of human bronchial epithelial BEP2D cells to NNK resulted in cell mali

SUBMITTER: Liu X 

PROVIDER: S-EPMC11889559 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature