The role of DYRK2 in primary liver cancers

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K09378
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Jikei University School of Medicine
• Principal Investigator: Oikawa Tsunekazu 東京慈恵会医科大学, 医学部, 講師 (20514491)
• Co-Investigator(Kenkyū-buntansha): 吉田 清嗣 東京慈恵会医科大学, 医学部, 教授 (70345312)
• Research Collaborator: Mashima Shiho ; Yogosawa Satomi
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 肝癌 / がん幹細胞

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.

Free Research Field

肝癌

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