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  • MicroRNA-34a overcomes HGF-mediated gefitinib resistance in EGFR mutant lung cancer cells partly by targeting MET.

MicroRNA-34a overcomes HGF-mediated gefitinib resistance in EGFR mutant lung cancer cells partly by targeting MET.

Cancer letters (2014-07-02)
Jian-Ya Zhou, Xi Chen, Jing Zhao, Zhang Bao, Xing Chen, Pei Zhang, Zhen-Feng Liu, Jian-Ying Zhou
ABSTRACT

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.

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Hepatocyte Growth Factor human, HGF, recombinant, expressed in NSO cells, suitable for cell culture
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Hepatocyte Growth Factor human, HGF, recombinant, expressed in Baculovirus infected High-5 cells, suitable for cell culture
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HGF mouse, recombinant, expressed in Hi-5 Insect cells, ≥95% (SDS-PAGE), ≥95% (HPLC)
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HGF human, recombinant, expressed in CHO cells, ≥97% (SDS-PAGE), ≥97% (HPLC)
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