| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| 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.
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