Transcriptional and phenotypical alterations associated with a gradual benzo[a]pyrene-induced transition of human bronchial epithelial cells into mesenchymal-like cells
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
38522766
DOI
10.1016/j.etap.2024.104424
PII: S1382-6689(24)00064-4
Knihovny.cz E-zdroje
- Klíčová slova
- 2,3,7,8-tetrachlorodibenzo-p-dioxin, Aryl hydrocarbon receptor, Benzo[a]pyrene, Epithelial-mesenchymal transition, Human bronchial epithelial cells,
- MeSH
- benzopyren * toxicita MeSH
- epitelové buňky * metabolismus MeSH
- lidé MeSH
- ligandy MeSH
- poškození DNA MeSH
- receptory aromatických uhlovodíků genetika metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- benzopyren * MeSH
- ligandy MeSH
- receptory aromatických uhlovodíků MeSH
The role of benzo[a]pyrene (BaP), a prominent genotoxic carcinogen and aryl hydrocarbon receptor (AhR) ligand, in tumor progression remains poorly characterized. We investigated the impact of BaP on the process of epithelial-mesenchymal transition (EMT) in normal human bronchial epithelial HBEC-12KT cells. Early morphological changes after 2-week exposure were accompanied with induction of SERPINB2, IL1, CDKN1A/p21 (linked with cell cycle delay) and chemokine CXCL5. After 8-week exposure, induction of cell migration and EMT-related pattern of markers/regulators led to induction of further pro-inflammatory cytokines or non-canonical Wnt pathway ligand WNT5A. This trend of up-regulation of pro-inflammatory genes and non-canonical Wnt pathway constituents was observed also in the BaP-transformed HBEC-12KT-B1 cells. In general, transcriptional effects of BaP differed from those of TGFβ1, a prototypical EMT inducer, or a model non-genotoxic AhR ligand, TCDD. Carcinogenic polycyclic aromatic hydrocarbons could thus induce a unique set of molecular changes linked with EMT and cancer progression.
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