Abstract
Cigarette smoke-induced protein aggregation damages the lung cells in emphysema and COPD; however, lung cancer cells continue to thrive, evolving to persist in the toxic environment. Here, we showed that upon the cigarette smoke condensate exposure, A549 lung cancer cells exhibit better survival and reduced level of protein aggregation when compared to non-cancerous Beas-2B and H-6053 cells. Our data suggests that upregulation of efflux pumps in cancer cells assists in reducing smoke toxicity. Specifically, we demonstrated that inhibition of the ABCG2 transporter in A549 by febuxostat or its downregulation by shRNA-mediated RNA interference resulted in a significant increase in protein aggregation due to smoke exposure.
Funder
Pennsylvania Department of Health
Publisher
Public Library of Science (PLoS)
Reference46 articles.
1. Content of toxic components of cigarette, cigarette smoke vs cigarette butts: A comprehensive systematic review;F Soleimani;Science of the Total Environment,2022
2. Reactive nitrogen species: Molecular mechanisms and potential significance in health and disease;MC Martínez;Antioxidants and Redox Signaling,2009
3. The role of reactive nitrogen species and cigarette smoke in activation of transcription factor NF-kappaB and implication to inflammatory processes;M Bar-Shai;The Journal of Physiology and Pharmacology,2006
4. Tobacco smoke: Involvement of reactive oxygen species and stable free radicals in mechanisms of oxidative damage, carcinogenesis and synergistic effects with other respirable particles;A Valavanidis;Int J Environ Res Public Health,2009
5. The etiologic origins for chronic obstructive pulmonary disease;X Huang;International Journal of COPD,2019