EMP3 is upregulated upon epithelial-mesenchymal transition and contributes to EGFR-tyrosine kinase inhibitor resistance in lung adenocarcinoma.

ABSTRACT: Tyrosine kinase inhibitors (TKIs) are a class of therapies used to target specific genetic mutations such as epidermal growth factor receptor (EGFR) mutations in cancer treatment. This study investigates the function of epithelial membrane protein 3 (EMP3) in EGFR-TKI resistance in lung adenocarcinoma (LUAD). Human LUAD cells HCC827 and H1975 were exposed to different doses of osimertinib or erlotinib to generate TKI-resistant cell lines. These cells exhibited increased expression of EMP3. EMP3 overexpression in parental cells significantly increased TKI resistance, as well as promoted proliferation, migration, and stem cell characteristics. Epithelial-mesenchymal transition (EMT) is a major cause for EMP3 upregulation, as overexpression of ZEB1 increased EMP3 expression. By contrast, inhi

SUBMITTER: Wang C 

PROVIDER: S-EPMC12278602 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature