Particulate Matter (PM
| Autor: | Claudia M, García-Cuellar, Miguel, Santibáñez-Andrade, Yolanda I, Chirino, Raúl, Quintana-Belmares, Rocío, Morales-Bárcenas, Ericka Marel, Quezada-Maldonado, Yesennia, Sánchez-Pérez |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Epithelial-Mesenchymal Transition
Lung Neoplasms Smad Proteins cancer hallmark epithelial–mesenchymal transition invasion complex mixtures Models Biological Article respiratory tract diseases Up-Regulation Gene Expression Regulation Neoplastic Transforming Growth Factor beta1 PM10 A549 A549 Cells Cell Movement embryonic structures TGFB1 Humans Neoplasm Invasiveness Particulate Matter Phosphorylation Signal Transduction |
| Zdroj: | International Journal of Molecular Sciences |
| ISSN: | 1422-0067 |
| Popis: | Air pollution presents a major environmental problem, inducing harmful effects on human health. Particulate matter of 10 μm or less in diameter (PM10) is considered an important risk factor in lung carcinogenesis. Epithelial–mesenchymal transition (EMT) is a regulatory program capable of inducing invasion and metastasis in cancer. In this study, we demonstrated that PM10 treatment induced phosphorylation of SMAD2/3 and upregulation of SMAD4. We also reported that PM10 increased the expression and protein levels of TGFB1 (TGF-β), as well as EMT markers SNAI1 (Snail), SNAI2 (Slug), ZEB1 (ZEB1), CDH2 (N-cadherin), ACTA2 (α-SMA), and VIM (vimentin) in the lung A549 cell line. Cell exposed to PM10 also showed a decrease in the expression of CDH1 (E-cadherin). We also demonstrated that expression levels of these EMT markers were reduced when cells are transfected with small interfering RNAs (siRNAs) against TGFB1. Interestingly, phosphorylation of SMAD2/3 and upregulation of SMAD induced by PM10 were not affected by transfection of TGFB1 siRNAs. Finally, cells treated with PM10 exhibited an increase in the capacity of invasiveness because of EMT induction. Our results provide new evidence regarding the effect of PM10 in EMT and the acquisition of an invasive phenotype, a hallmark necessary for lung cancer progression. |
| Databáze: | OpenAIRE |
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