Snail Induces Mesenchymal Transition and Promotes EGFR TKI Resistance in NSCLC Cells Harboring EFGR Kinase Domain Mutations

Lung cancer is the leading cause of cancer related death, accounting for one third of all deaths from cancer worldwide. About 85-90% of lung cancers are non-small cell lung cancers (NSCLCs). Molecular targeted therapies such as epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) provide an effective treatment option for oncogene addicted NSCLC. However, the development of resistance to EGFR TKIs continues to be the major limitation in the treatment of NSCLC. Resistance to EGFR TKIs has been associated with the loss of canonical epithelial protein E-cadherin, suggesting involvement of epithelial to mesenchymal transition (EMT) in conferring EGFR TKI resistance. Transcription factors that regulate EMT may play a critical role in altering drug sensitivity of cancer cells. In this review we investigated the role of transcription factor SNAIL in affecting sensitivity of EGFR mutant NSCLC to EGFR TKIs