Date on Master's Thesis/Doctoral Dissertation
12-2018
Document Type
Master's Thesis
Degree Name
M.S.
Department
Pharmacology and Toxicology
Degree Program
Pharmacology and Toxicology, MS
Committee Chair
Ceresa, Brian P.
Committee Co-Chair (if applicable)
States, J. Christopher
Committee Member
States, J. Christopher
Committee Member
Hood, Joshua L.
Committee Member
Watson, Walter H.
Committee Member
Wise, Sr. John P.
Author's Keywords
arsenic; EGFR; metal; trafficking
Abstract
The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase localized on the cell surface. Overexpression of EGFR has been used as biomarkers for many different types of cancers, including lung cancer. There is a strong association between arsenic and lung cancer development, although the mechanism is unclear. We hypothesize that chronic exposure of “a physiologically relevant” level of arsenite disrupts the EGFR endocytic trafficking. The goal of this project is to identify molecular mechanisms and roles of chronic arsenite-induced EGFR overexpression in lung cancer development. A non-malignant human bronchial epithelial cell line, Beas-2B cells were exposed to 100 nM sodium arsenite for 24 weeks. The chronic arsenite-treated cells had increased EGFR protein expression levels and activity, increased transcription levels of TGFα, and altered the distribution of the EGFR. In conclusion, the impact of chronic arsenite exposure on the EGFR signaling axis can explain arsenite-induced overexpression of the EGFR.
Recommended Citation
Kim, Christine, "Assessing the role of arsenite in disrupting the EGFR signaling axis." (2018). Electronic Theses and Dissertations. Paper 3131.
https://doi.org/10.18297/etd/3131