| Project/Area Number |
26462613
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
KONDO ATSUSHI 札幌医科大学, 医学部, 講師 (40457718)
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| Co-Investigator(Kenkyū-buntansha) |
高野 賢一 札幌医科大学, 医学部, 准教授 (70404689)
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| Co-Investigator(Renkei-kenkyūsha) |
KOJIMA TAKASHI 札幌医科大学, 医学部, 教授 (30260764)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 咽頭がん / 細胞極性 / YAP / LSR / PAR3 / ASPP2 / HDAC / タイト結合 / 接着分子 / Par3 / ZEB1 / .咽頭がん |
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| Outline of Final Research Achievements |
The first, in pharyngeal squamous cell carcinomas (PSCC), a hippo pathway key molecule YAP which contributed to organogenesis signaling, was positive in the nuclei of all cancer cells. The changes in expression and localization of LSR (lipolysis-stimulated lipoprotein receptor) which was regulated by YAP were observed during the malignancy. In LSR-knockdown cancer cell line, upregulation of cell invasion and migration was observed. The next, epithelial cell polarity molecules PAR3 and the regulator ASPP2 (apoptosis stimulating proteins of p53-2) were upregulated in PSCC than dysplasia. Inhibitors of HDACs (histone deacetylases) which upregulated in PSCC, induced expression of PAR3 and ASPP2 and inhibited cancer cell invasion and migration. In conclusion, the regulation of epithelial cell polarity molecules LSR, PAR3 and ASPP2 and organogenesis signaling YAP may be an important to prevent invasion/metastasis of PSCC.
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