28PD - HOTAIR induces EGFR-TKIs resistance in non-small cell lung cancer via epithelial-mesenchymal transition

Date 17 December 2016
Event ESMO Asia 2016 Congress
Session Basic science and translational research
Topics Thoracic malignancies
Translational Research
Presenter Ningning Cheng
Citation Annals of Oncology (2016) 27 (suppl_9): ix9-ix18. 10.1093/annonc/mdw574
Authors N. Cheng1, Q. Wang2, W. Cai3, S. Ren3, X. Li3, C. Zhao3, C. Zhou3
  • 1Oncology Cencer, 1st Shanghai People's Hospital, 200080 - Shanghai/CN
  • 2Medical Oncology, Shanghai Pulmonary Hospital, Tongji University, 200080 - Shanghai/CN
  • 3Medical Oncology, Shanghai Pulmonary Hospital, Tongji University, 200433 - Shanghai/CN

Abstract

Background

Previous research found that HOTAIR, a long non-coding RNA, is aberrantly expressed and associated with tumor invasion, metastasis and chemo-resistance in many cancers. The aim of this study was to investigate the role of HOTAIR in resistance of EGFR-TKIs in NSCLC.

Methods

HOTAIR expression level was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) in NSCLC cell lines or tumor tissues. A total of 52 samples with EGFR-mutant and EGFR-TKI-sensitive NSCLCs, 42 with acquired resistance and 46 with primary resistance to EGFR-TKIs were analyzed. The effect of HOTAIR on cell proliferation and apoptosis was investigated by CCK-8 and flow cytometry assays. The expression of EMT proteins was assessed by western blot.

Results

HOTAIR was significantly down-regulated in lung cancer cells (PC9/R, H1975, H1299 and A549) and patients with primary and acquired resistance to EGFR-TKIs. In the clinical setting, high levels of HOTAIR expression was significantly correlated with longer progression-free survival (PFS; P 

Conclusions

HOTAIR expression was associated with primary and acquired resistance to EGFR-TKIs and could regulate cell proliferation through activating cell apoptosis and EMT, which suggest that HOTAIR might act as a biomarker to predict the EGFR-TKI resistance.

Clinical trial indentification

Legal entity responsible for the study

CSCO

Funding

CSCO

Disclosure

All authors have declared no conflicts of interest.