EGFR exon 19-deletion aberrantly regulate ERCC1 expression that may partly impaired DNA damage repair ability in non-small cell lung cancer.

ABSTRACT:

Background

Epidermal growth factor receptor (EGFR) activating mutations are usually associated with DNA damage repair (DDR) deficiency. However, the precise mechanism has remained elusive. In this study, we aimed to investigate whether EGFR exon 19 deletion mutation downstream signals contributed to DDR deficiency by downregulation of excision repair cross-complementation group-1 (ERCC1), a key factor in DDR, expression and function.

Methods

We first measured cell survival, DNA damage (γ-H2AX foci formation) and damage repair (ERCC1 and RAD51 foci formation) ability in response to DNA cross-linking drug in EGFR exon 19 deletion and EGFR wild-type cells separately. We then investigated the involvement of EGFR downstream signals in regulating ERCC1 expression and function in E

SUBMITTER: Zhang L 

PROVIDER: S-EPMC6996978 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature