2010 Fiscal Year Final Research Report
Constitutive activation of Stat3 reveals a critical role in UVB-induced epithelial carcinogenesis
| Project/Area Number |
20591322
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Kochi University |
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Principal Investigator |
YOKOGAWA Maki Kochi University, 教育研究部・医療学系, 助教 (40346721)
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| Co-Investigator(Kenkyū-buntansha) |
MIYOSHI Ken 高知大学, 教育研究部・医療学系, 助教 (20274392)
SANO Shigetoshi 高知大学, 教育研究部・医療学系, 教授 (80273621)
TERAISHI Mika 高知大学, 医学部附属病院, 医員 (40437736)
SHIGA Takeo 高知大学, 教育研究部・医療学系, 助教 (70444768)
IKEDA Mitsunori 高知県立大学, 健康長寿センター, 教授 (70212785)
TAKAISHI Mikiro 高知大学, 教育研究部・医療学系, 助教 (10303223)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 紫外線 / 発癌 / 表皮角化細胞 / Stat3 |
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| Research Abstract |
Constitutive activation of Stat3 has been found in many human malignancies including skin cancer. Here we examined whether inhibition of Stat3 signaling affected the progression of UVB-induced cancer in Stat3-constitutive active mice (K5. Stat3C). We used a small compound Stat3-inhibitor, named STA-21 (ochronomycinone). Pretreatment of topical STA-21 application delayed the appearance of UVB-induced cancer. Furthermore, STA-21 markedly inhibited the growth of cancer at the progressive stage, whereas vehicle-treated control mice developed invasive cancer. These results indicated that Stat3 inhibition decreased the UVB-induced carcinogenic process, and therefore, could be a novel therapy for actinic keratosis and SCC.
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