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Microenvironment and autophagy in arsenic lung tumorigenesis | 54462
Journal of Clinical Toxicology

Journal of Clinical Toxicology
Open Access

ISSN: 2161-0495

Microenvironment and autophagy in arsenic lung tumorigenesis


6th Global Summit on Toxicology & Applied Pharmacology

October 17-19, 2016 Houston, USA

Gang Chen

University of Kentucky, USA

Posters & Accepted Abstracts: J Clinic Toxicol

Abstract :

The alterations in lung microenvironment upon chronic arsenic exposure may contribute to arsenic lung tumorigenesis. Immune cells play an important role in mediating the microenvironment in the lungs. Our previous work has shown that long-term arsenic exposure induces transformation of lung epithelial cells in which autophagy functions as a protective mechanism. However, the crosstalk between epithelial cells and immune cells/microenvironment upon arsenic exposure is not clear. Recently using a co-culture system with epithelial cells and immune cells, we determined that long-term arsenic exposure altered the phenotype of certain immune cells. Blocking the alteration decreases arsenic-induced transformation of epithelial cells. In addition, the phenotype changes in immune cells upon arsenic exposure decreases autophagy activity, which may account for increased cell transformation of epithelial cells with co-culture of the immune cells.

Biography :

Email: gangchen6@uky.edu

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