HCC-derived EGFR mutants are functioning, EGF-dependent, and erlotinib-resistant.

ABSTRACT:

Background

Epidermal growth factor receptor (EGFR) has emerged as an important therapeutic target. Overexpression of EGFR is frequently observed in hepatocellular carcinoma (HCC) and EGFR activation has been proven to be a potential determinant of primary resistance of HCC cells to sorafenib. In our previous study, we found 13 missense mutations in EGFR exon 19-23 from hepatocellular carcinoma (HCC) tissues, but the functions of these mutations have not been determined. This study aims to determine the kinase activity and sensitivity to erlotinib, a 1st-generation EGFR-tyrosine kinase inhibitor (TKI), of seven HCC-derived mutants (K757E, N808S, R831C, V897A, P937L, T940A, and M947T).

Results

Using transduction of pBabe-puro retroviral vector with or without EGFR, we construc

SUBMITTER: Sueangoen N 

PROVIDER: S-EPMC7076995 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature