2017 Fiscal Year Final Research Report
Elucidation of factors associating with chemoresistance in EGFR-TKI resistant lung adenocarcinoma
Project/Area Number |
16K19073
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Human pathology
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Research Institution | Tohoku University |
Principal Investigator |
Saito Ryoko 東北大学, 医学系研究科, 助教 (30733349)
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Project Period (FY) |
2016-04-01 – 2018-03-31
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Keywords | lung adenocarcinoma / EGFR-TKI resistance / chemoresistance / HIF-1α / p22phox |
Outline of Final Research Achievements |
Chemotherapy is broadly used for the patients with EGFR-TKI (epidermal growth factor receptor-tyrosine kinase inhibitors) resistant lung adenocarcinoma. This study aimed to elucidate the mechanism associating with chemoresistance and EGFR-TKI resistance. According to the microarray using EGFR-TKI resistant lung adenocarcinoma cell line, we postulated that p22phox/ HIF-1α (hypoxia inducible factor-1α) pathway might be result in chemoresistance and EGFR-TKI resistance via induction of EMT (epithelial-mesenchymal transition). Our study showed that p22phox and HIF-1α expressions were elevated in some EGFR-TKI resistant lung adenocarcinoma cell line, and that in these cell line p22phox induced HIF-1α gene expression following to induction of EMT and chemoresistance. Our results may provide the first evidence that targeting p22phox/ HIF-1α could be a new therapeutic strategy to enhance the chemosensitivity in EGFR-TKI resistant lung adenocarcinoma.
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Free Research Field |
人体病理学
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