EGFR mediated arsenic induced carcinogenesis: An overview

EGFR is a receptor tyrosine kinase (RTK) localized on the cell face (Fig. 1). As one of the erbb family receptors (EGFR, erbb2, erbb3, and erbb4), EGFR is actuated by specific ligands, and there are 7 endogenous EGFR ligands (epidermal growth factor (EGF), transubstantiating growth factor-α (tgfα), HB-EGF, amphiregulin (AREG), betacellulin (BTC), epigen (EPGN), epiregulin (EREG)). Arsenic is a potent poison, due to its lack of color, taste and odor. Also, the symptoms from arsenic poisoning are very similar to the symptoms of food poisoning, thus rendering it nearly untraceable without sophisticated analytical procedures. Proposed mechanisms of arsenic- convinced carcinogenesis include oxidative stress, epigenetic changes including histone revision, mirna expression, and DNA methylation, aneuploidy, and activation of oncogenic pathways, similar as the epidermal growth factor receptor (EGFR). The overexpression of EGFR and its association with a poor prognostic can be explained by increased spots for the ligands to bind to the receptors, leading to enhanced downstream signaling events, similar as proliferation. An increase in conflation of ligands above the rudimentary situations also triggers improvement of the EGFR- convinced activation of proliferative pathways. High situations of EGFR ligands, including EGF, tgfα, AREG, and BTC, were observed in cancers.