The role of DYRK2 in primary liver cancers
| Project/Area Number |
16K09378
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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 |
Gastroenterology
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
吉田 清嗣 東京慈恵会医科大学, 医学部, 教授 (70345312)
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| Research Collaborator |
Mashima Shiho
Yogosawa Satomi
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 肝癌 / がん幹細胞 / 癌幹細胞 / 転移 / 肝幹細胞 / 肝発生 |
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| Outline of Final Research Achievements |
The only curative treatments for liver cancers are surgical resection for early-stage patients. However, most patients are diagnosed at advanced stages. For the treatment of advanced HCC patients with unresectable tumors, transcatheter arterial chemoembolization and systemic chemotherapy,including TKI, but the effects are limited. Therefore, the identification of novel molecules that can become targets for future therapies is urgently needed.
We have reported that dual-specificity tyrosine-regulated kinase 2 (DYRK2) functions as a tumor suppressor by regulating cell survival, differentiation, proliferation and apoptosis. In this study, we found that patients whose liver cancers were expressed with low levels of DYRK2 had a significantly worse overall survival than those with higher levels. Overexpression of DYRK2 inhibited cell proliferation and tumor growth and induced apoptosis. The forced expression of DYRK2 may become a potential target for gene therapy of liver cancer.
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| Academic Significance and Societal Importance of the Research Achievements |
上記の結果は以下の論文に掲載され、今後の肝癌の新規治療法開発に向けた展望が期待される。Yokoyama-Mashima S, Yogosawa S, Kanegae Y, Hirooka S, Yoshida S, Horiuchi T, Ohashi T, Yanaga K, Saruta M, Oikawa T, Yoshida K. Forced expression of DYRK2 exerts anti-tumor effects via apoptotic induction in liver cancer. Cancer Lett. 451,100-109,2019
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Report
(4 results)
Research Products
(7 results)
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[Journal Article] Forced expression of DYRK2 exerts anti-tumor effects via apoptotic induction in liver cancer.2019
Author(s)
Yokoyama-Mashima S, Yogosawa S, Kanegae Y, Hirooka S, Yoshida S, Horiuchi T, Ohashi T, Yanaga K, Saruta M, Oikawa T, Yoshida K.
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Journal Title
Cancer Lett
Volume: 451
Pages: 100-109
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Comprehensive analysis of The Cancer Genome Atlas reveals a unique gene and non-coding RNA signature of fibrolamellar carcinoma.2017
Author(s)
Dinh TA, Vitucci EC, Wauthier E, Graham RP, Pitman WA, Oikawa T, Chen M, Silva GO, Greene KG, Torbenson MS, Reid LM, Sethupathy P.
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Journal Title
Sci Rep.
Volume: 17
Issue: 1
Pages: 44653-44653
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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