Transcriptional upregulation of c-MYC by AXL confers epirubicin resistance in esophageal adenocarcinoma.

ABSTRACT: AXL receptor tyrosine kinase is overexpressed in esophageal adenocarcinoma (EAC) and several other types of malignancies; hence, it may be a valuable therapeutic target. Herein, we investigated the role of AXL in regulating c-MYC expression and resistance to the chemotherapeutic agent epirubicin in EAC. Using in vitro EAC cell models, we found that AXL overexpression enhances epirubicin resistance in sensitive cells. Conversely, genetic knockdown or pharmacological inhibition of AXL sensitizes resistant cells to epirubicin. Notably, we showed that inhibition or knockdown of c-MYC markedly sensitizes AXL-dependent resistant cells to epirubicin, and our data demonstrated that AXL promotes epirubicin resistance through transcriptional upregulation of c-MYC. We showed that AXL overexpression s

SUBMITTER: Hong J 

PROVIDER: S-EPMC6275285 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature