Study for the tumor suppressor network through STAT3 regulation in drug-resistance of oral squamous cell carcinoma

2015 Fiscal Year Final Research Report

• Project/Area Number: 25463124
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: National Hospital Organization, Kyushu Medical Center (Clinical Institute) (2015); Fukuoka Dental College (2013-2014)
• Principal Investigator: Ozeki Satoru 独立行政法人国立病院機構九州医療センター(臨床研究センター), その他部局等, その他 (80117077)
• Co-Investigator(Kenkyū-buntansha): HASHIMOTO KENICHIRO 福岡歯科大学, 歯学部, 講師 (00412619) ; KIYOSHIMA TAMOTSU 九州大学, 大学院歯学研究科, 教授 (20264054)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 口腔扁平上皮癌 / STAT3 / アポトーシス / 薬剤抵抗性 / 腫瘍細胞活性ネットワーク / 腫瘍増殖活性化 / 腫瘍増殖抑制

Outline of Final Research Achievements

The overcome of the resistance of such tumors to the chemotherapeutic agents is required to improve the tumor specificity for OSCC. We studied the tumor suppressor network through regulation of STAT3 in drug-resistance of oral squamous cell carcinoma (OSCC). The high IL-6 expression OSCCs showed highly expression of phosphorylated STAT3 and correlated closely with cervical lymph node metastases, preoperative chemoradiotherapy resistance and unfavourable prognosis. Because V-ATPase plays a critical role in tumor progression, the effects of a V-ATPase inhibitor on the proliferation and apoptosis of OSCC were investigated. The treatment of V-ATPase inhibitor combined with a histone deacetylase inhibitor changed STAT3 phosphorylation in the drug-resistant OSCC cells. These cells became more susceptible to the V-ATPase inhibitor. These results suggested that the regulation of activated STAT3 in the cancer cells could help improve poor response to chemotherapy and unfavorable prognosis.

Free Research Field

外科系歯学　臨床腫瘍学