Journal
CANCER LETTERS
Volume 351, Issue 2, Pages 265-271Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2014.06.010
Keywords
miR-34a; Lung cancer; HGF; MET; Gefitinib resistance
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Funding
- National Natural Science Foundation of China [81101768]
- State Scholarship Fund of China [201308330145]
- Key Personnel of Zhejiang Medicine and Health Platform [2012RCA025]
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In non-small-cell lung cancer (NSCLC) that harbours an activating epidermal growth factor receptor (EGFR) mutation, over-expression of hepatocyte growth factor (HGF) is an important mechanism involved in the acquired resistance to EGFR-tyrosine kinase inhibitors (TKIs) by restoring activity of the PI3K/Akt pathway via phosphorylation of MET. In our study, we found that the forced expression of miR-34a inhibited cell growth and induced apoptosis partly by targeting MET in HGF-induced gefitinib-resistant HCC827 and PC-9 cells. Furthermore, dramatic tumour regression was observed in the miR-34a plus gefitinib group in HGF-induced gefitinib resistant mouse xenograft models. This study demonstrates for the first time that miR-34a rescues HGF-induced gefitinib resistance in EGFR mutant NSCLC cells. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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