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• W2912921222 abstract "Enhancing the chemosensitivity in the patients with epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistant lung adenocarcinoma (LUAD) is pivotal in achieving their successful therapeutic outcome. We aimed to explore the mechanisms regarding the development of therapeutic resistance to chemotherapy in EGFR-TKI resistant LUAD. Methods: Microarray analysis lead to potential involvement of p22phox, which was abundantly expressed in the cell lines harboring EGFR-TKI resistance and chemoresistance, and was known to regulate several important chemoresistance-associated factors such as hypoxia inducible factor-1α (HIF-1α) and epithelial-mesenchymal transition (EMT). We compared the status of p22phox with that of chemoresistance, HIF-1α expression and EMT in LUAD cell lines. We immunolocalized p22phox in the specimens of lung cancer patients.p22phox and HIF-1α mRNAs were significantly elevated in the cells harboring EMT and chemoresistance. p22phox knockdown enhanced chemosensitivity and reduced the expression of HIF-1α and EMT-associated factors. HIF-1α knockdown enhanced the chemosensitivity, while HIF-1α transfection induced EMT and chemoresistance in these cell lines. All LUAD patients with T790M mutation were associated with abundant p22phox immunoreactivity in carcinoma cells.The analysis of p22phox in lung carcinoma tissues could provide new insights into the selection of chemotherapy for the patients with EGFR-TKI resistant LUAD." @default.
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• W2912921222 date "2019-02-01" @default.
• W2912921222 modified "2023-09-27" @default.
• W2912921222 title "The correlation of p22phox and chemosensitivity in EGFR-TKI resistant lung adenocarcinoma" @default.
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• W2912921222 doi "https://doi.org/10.18632/oncotarget.26637" @default.
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