| Project/Area Number |
15K06844
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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 |
Tumor biology
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| Research Institution | Nihon University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
YAMAGUCHI Kenya 日本大学, 医学部, 准教授 (00297813)
MATSUMOTO Taro 日本大学, 医学部, 教授 (50366580)
ENDO Morito 八戸学院大学, 健康医療学部, 学部長/教授 (10399735)
KATAKAWA Mayumi 日本大学, 医学部, 研究協力員 (60645696)
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| Research Collaborator |
IKEDA Jin
TREMBLAY Johanne
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| Project Period (FY) |
2015-10-21 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | HCaRG / COMMD5 / 腎細胞癌 / EGFR / 間葉上皮移行 / 予後予測因子 / バイオマーカー / 尿細管上皮細胞 |
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| Outline of Final Research Achievements |
Hypertension-related, calcium-regulated gene (HCaRG/COMMD5) is highly expressed in renal proximal tubules and accelerates tubular repair by facilitating re-differentiation of injured tubular cells. Sustained hyper-proliferation and de-differentiation are important hallmarks of tumor progression. Cancer cells overexpressing HCaRG maintain a more differentiated phenotype. Its overexpression in mouse renal cell carcinomas (RCC) led to smaller tumor size with less tumor vascularization in a homograft tumor model. Mechanistically, HCaRG promotes de-phosphorylation of EGFR, HER2 and ErbB3. ERK1/2and AKT which mediate ErbB signaling pathways are inactivated by HCaRG. In addition, HCaRG is underexpressed in human RCCs and more expressed in normal kidneys of patients with favorable prognosis. Taken together, our data suggest a role for HCaRG in the inhibition of tumor progression as a natural inhibitor of the ErbB signals in cancer and as a potential prognostic marker for RCCs.
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