biostudies-literatureJin QChinese Medicine Scientific Projects of Zhejiang Province6633867https://www.ebi.ac.uk/biostudies/studies/S-EPMC7946473biostudies-literatureUnknown2021<h4>Background</h4>Acquired resistance occurred in the majority of nonsmall cell lung cancer (NSCLC) patients receiving epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) therapy, and this may be related to the activation of the HIF-1 pathway. Therefore, we examined the influence of the hypoxia-inducible factor-1 (HIF-1) pathway inhibition on the sensitivity of HCC827 gefitinib-resistant (HCC827 GR) cells with MET amplification to gefitinib.<h4>Methods</h4>We established HCC827 GR cell line with MET amplification and set four groups with different treatment. An MTT assay, a colony formation analysis, and a wound healing assay were performed to determine the sensitivity change of HCC827 GR cells after different treatments. HIF-1<i>α</i>, p-EGFR, and p-Met levels were detected with western blot. Correlations among HIF-1<i>α</i>, p-EGFR, and p-Met levels of HCC827 GR cells with different treatments were analyzed with Pearson's correlation analysis.<h4>Results</h4>HIF-1 inhibitor YC-1 enhanced the sensitivity of HCC827 GR cells to gefitinib. p-Met level was correlated with HIF-1<i>α</i> level, while there was no correlation between p-Met level and p-EGFR level.<h4>Conclusion</h4>HIF-1 inhibitor YC-1 is able to reverse the acquired resistance of HCC827 GR to gefitinib, and the regulation of the HIF-1 pathway on MET may be one of the mechanisms.Oxidative medicine and cellular longevityHIF-1 Inhibitor YC-1 Reverses the Acquired Resistance of EGFR-Mutant HCC827 Cell Line with MET Amplification to Gefitinib.PMC79464732016KYB0532018ZA020Zheng JHuang FJin QChen MXu XJiang NfalseHIF-1 Inhibitor YC-1 Reverses the Acquired Resistance of EGFR-Mutant HCC827 Cell Line with MET Amplification to Gefitinib.<h4>Background</h4>Acquired resistance occurred in the majority of nonsmall cell lung cancer (NSCLC) patients receiving epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) therapy, and this may be related to the activation of the HIF-1 pathway. Therefore, we examined the influence of the hypoxia-inducible factor-1 (HIF-1) pathway inhibition on the sensitivity of HCC827 gefitinib-resistant (HCC827 GR) cells with MET amplification to gefitinib.<h4>Methods</h4>We established HCC827 GR cell line with MET amplification and set four groups with different treatment. An MTT assay, a colony formation analysis, and a wound healing assay were performed to determine the sensitivity change of HCC827 GR cells after different treatments. HIF-1<i>α</i>, p-EGFR, and p-Met levels were detected with western blot. Correlations among HIF-1<i>α</i>, p-EGFR, and p-Met levels of HCC827 GR cells with different treatments were analyzed with Pearson's correlation analysis.<h4>Results</h4>HIF-1 inhibitor YC-1 enhanced the sensitivity of HCC827 GR cells to gefitinib. p-Met level was correlated with HIF-1<i>α</i> level, while there was no correlation between p-Met level and p-EGFR level.<h4>Conclusion</h4>HIF-1 inhibitor YC-1 is able to reverse the acquired resistance of HCC827 GR to gefitinib, and the regulation of the HIF-1 pathway on MET may be one of the mechanisms.2021-01-01T00:00:00Z20212025-04-18T23:10:22.808Z2025-04-07T10:43:46.494ZS-EPMC79464733376317110.1155/2021/6633867