A role of microRNA-mediated regulatory mechanism of WT1 in oncogenesis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460685
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Laboratory medicine
• Research Institution: Osaka University
• Principal Investigator: TATSUMI NAOYA 大阪大学, 医学(系)研究科(研究院), 寄附講座助教 (60512960)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: microRNA / WT1遺伝子 / 白血病 / Zbtb7a遺伝子 / 肺癌

Outline of Final Research Achievements

In the present study, we showed that knockout mice for miR-125a, which directly targets and suppresses the expression of WT1 gene, developed myeloproliferative disorder (MPD) characterized by expansion of myeloid cells. Furthermore, the incidence and severity of MPD were lower in miR-125a (-/-) mice than in miR-125a (+/-) mice, indicating the operation of compensatory mechanisms for the complete loss of miR-125a. MiR-486 was occasionally induced in compete loss of miR-125a and, resulting in the cancellation of MPD occurrence. Moreover, we showed that Zbtb7a was a direct target for miR-125a and that miR-125a played an important role in oncogenesis through the regulation of two oncogenes, WT1 and Zbtb7a.

Free Research Field

医歯薬学　境界医学・病態検査学