Cisplatin sensitivity is enhanced in non-small cell lung cancer cells by regulating epithelial-mesenchymal transition through inhibition of eukaryotic translation initiation factor 5A2.

Abstract:

BACKGROUND:Epithelial-mesenchymal transition (EMT) has been believed to be related with chemotherapy resistance in non-small cell lung cancer (NSCLC). Recent studies have suggested eIF5A-2 may function as a proliferation-related oncogene in tumorigenic processes. METHODS:We used cell viability assays, western blotting, immunofluorescence, transwell-matrigel invasion assay, wound-healing assay combined with GC7 (a novel eIF5A-2 inhibitor) treatment or siRNA interference to investigate the role of eIF5A-2 playing in NSCLC chemotherapy. RESULTS:We found low concentrations of GC7 have little effect on NSCLC viability, but could enhance cisplatin cytotoxicity in NSCLC cells. GC7 also could reverse mesenchymal phenotype in NCI-H1299 and prevented A549 cells undergoing EMT after TGF-β1 inducement. eIF5A-2 knockdown resulted in EMT inhibition. CONCLUSION:Our data indicated GC7 enhances cisplatin cytotoxicity and prevents the EMT in NSCLC cells by inhibiting eIF5A-2.

journal_name

BMC Pulm Med

journal_title

BMC pulmonary medicine

authors

Xu G,Yu H,Shi X,Sun L,Zhou Q,Zheng D,Shi H,Li N,Zhang X,Shao G

doi

10.1186/1471-2466-14-174

subject

Has Abstract

pub_date

2014-11-07 00:00:00

pages

174

issn

1471-2466

pii

1471-2466-14-174

journal_volume

14

pub_type

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