2015 Fiscal Year Final Research Report
Elucidate the mechanism of anti-cancer drug resistance caused by inhibitor apoptosis protein(IAP) and development of novel therapeutic strategy
Project/Area Number |
26861737
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Surgical dentistry
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Research Institution | Kumamoto University |
Principal Investigator |
NAGATA MASASHI 熊本大学, 医学部附属病院, 非常勤診療医師 (10635791)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Keywords | 抗がん剤耐性 / アポトーシス / 腫瘍周囲環境 |
Outline of Final Research Achievements |
We have reported the importance of cellular inhibitor of apoptosis 2 (cIAP2) using 5FU-resistant oral squamous cell carcinoma cell line, which we establish for 2 years 5FU treatment. We presented treatment-resistant and poor prognosis was due to cIAP2 high expression. To analyze of cIAP2 regulator, we found relevance of miR-30a overexpression and apoptosis inhibition. In additon, an overexpression of extracellular matrix molecule fibronectin activate of survival regulator and confers cell adhesion-mediated drug resistance against 5-FU. Furthermore, we reported tumour-associated macrophages (TAMs) are a potential biomarker for predicting the clinical response to 5-FU-based chemoradiotherapy, and the expression status of the cancer-associated fibroblasts and TAMs may be useful for making treatment decisions to improve the survival of OSCC patients.
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Free Research Field |
抗がん剤耐性
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