Knockdown of annexin A5 restores gefitinib sensitivity by promoting G2/M cell cycle arrest.

ABSTRACT:

Background

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, including gefitinib, are first-line drugs against advanced non-small cell lung cancer with activating EGFR mutations. However, the development of resistance to such drugs is a major clinical challenge.

Methods

The role of annexin A5 in resistance to EGFR tyrosine kinase inhibitors was investigated by qPCR and western blot of relevant molecules, by CCK8 and EdU assay of cell proliferation and viability, by annexin V/propidium iodide assay of apoptosis and cell cycle distribution, by JC-1 assay of mitochondrial integrity, and by xenograft assay of tumorigenicity.

Results

We found that annexin A5 is upregulated in gefitinib-resistant cell lines, as well as in clinical specimens resistant to EG

SUBMITTER: Zhou J 

PROVIDER: S-EPMC5963077 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature