Elucidate the mechanism of anti-cancer drug resistance caused by inhibitor apoptosis protein(IAP) and development of novel therapeutic strategy

2015 Fiscal Year Final Research Report

• Project/Area Number: 26861737
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Surgical dentistry
• 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)
• Project Period (FY): 2014-04-01 – 2016-03-31
• 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.

Free Research Field

抗がん剤耐性