Elucidation of factors associating with chemoresistance in EGFR-TKI resistant lung adenocarcinoma
Project/Area Number |
16K19073
|
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)
|
Project Period (FY) |
2016-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | lung adenocarcinoma / EGFR-TKI resistance / chemoresistance / HIF-1α / p22phox / 化学療法耐性 / EMT / ヒト肺腺癌 / EGFR-TKI耐性 / 病理学 / 癌 |
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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Report
(3 results)
Research Products
(3 results)