Epsin3 promotes non-small cell lung cancer progression via modulating EGFR stability.

ABSTRACT:

Background

The abnormal expression and overactivation of the epidermal growth factor receptor (EGFR), a typical cancer marker for non-small cell lung cancer (NSCLC), are closely related to the tumorigenesis and progression of NSCLC. However, the endocytosis mechanism of EGFR in lung cancer is not yet known. Epsin3 (EPN3), a member of the endocytic adaptor protein family, is essential for the endocytosis of multiple receptors. In this study, we aimed to investigate the role of EPN3 in modulating EGFR function, its effects on NSCLC progression, and its potential involvement in tyrosine kinase inhibitor (TKI) resistance, which remains a significant hurdle in NSCLC treatment.

Results

Our findings revealed that the expression of EPN3 is significantly up-regulated in NSCLC patient

SUBMITTER: Su H 

PROVIDER: S-EPMC11800460 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature