Exogenous hydrogen sulfide donor NaHS alleviates nickel-induced epithelial-mesenchymal transition and the migration of A549 cells by regulating TGF-β1/Smad2/Smad3 signaling
| Autor: | Meng-Juan Ye, Jiahui Li, Meng-Ping Yu, Hanning Yu, Tong Shen, Qi-Xing Zhu, Cheng-Fan Zhou, Da-Long Yang, Feipeng Chen, Haopei Wang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
MAPK/ERK pathway
Epithelial-Mesenchymal Transition Lung Neoplasms Health Toxicology and Mutagenesis 0211 other engineering and technologies Cystathionine beta-Synthase Smad2 Protein 02 engineering and technology Sulfides 010501 environmental sciences 01 natural sciences Transforming Growth Factor beta1 Cell Movement Nickel Humans Hydrogen Sulfide Smad3 Protein Epithelial–mesenchymal transition Protein kinase A Carcinogen 0105 earth and related environmental sciences A549 cell 021110 strategic defence & security studies biology Chemistry Cystathionine gamma-Lyase Public Health Environmental and Occupational Health Cell migration General Medicine Pollution Cystathionine beta synthase Cell biology A549 Cells Sulfurtransferases biology.protein Signal transduction Signal Transduction |
| Zdroj: | Ecotoxicology and Environmental Safety. 195:110464 |
| ISSN: | 0147-6513 |
| DOI: | 10.1016/j.ecoenv.2020.110464 |
| Popis: | Nickel compounds are known to be common environmental and occupational carcinogens which also promote the migration of lung cancer cells. However, the molecular mechanism yet remains to be clarified. Hydrogen sulfide (H2S) is involved in cancer biological processes. However, the exact effect and functionality of H2S on nickel, towards the promotion of the migration ability of lung cancer cells, remains to be unknown. In this study, we have found that the nickel chloride (NiCl2) treatment significantly downregulates the protein levels of endogenous H2S enzyme cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE) and 3-Mercaptopyruvate sulfurtransferase (3-MST). A correlation between NiCl2-induced epithelial-mesenchymal transition (EMT) and the migration ability of lung cancer A549 cells has been observed. Exogenous H2S donor, sodium hydrogen sulfide (NaHS) (100 μmol/L), can reverse NiCl2-induced EMT as well as the migration ability of A549 cells. NiCl2 treatment is able to upregulate the protein level of transforming growth factor-β1 (TGF-β1), p-Smad2, p-Smad3, p-JNK, p-ERK and p-P38 in a time-dependent fashion, indicating that both TGF-β1/Smad2/Smad3 and mitogen-activated protein kinase (MAPK) signaling cascades (a non-Smad pathway) may play essential roles in NiCl2-dependent EMT as well as cell migration of human lung cancer cells. Furthermore, exogenous NaHS alleviates the NiCl2-induced EMT and the migration ability of A549 cells only by regulating TGF-β1/Smad2/Smad3, rather than the MAPK, signaling pathway. These results indicate that the exogenous administration of NaHS might be a potential therapeutic strategy against nickel-induced lung cancer progression. |
| Databáze: | OpenAIRE |
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