| 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)
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| 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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