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2017 Fiscal Year Final Research Report

Molecular basis of the oncogenic effects of novel oncogene candidates, TRB family members

Research Project

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Project/Area Number 15K07937
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Biological pharmacy
Research InstitutionNagoya City University

Principal Investigator

Hayashi Hidetoshi  名古屋市立大学, 大学院薬学研究科, 教授 (80198853)

Project Period (FY) 2015-04-01 – 2018-03-31
KeywordsTRB3 / TRB1 / p53 / EMT / TGF-beta / がん幹細胞 / FOXO1 / CD44
Outline of Final Research Achievements

Overexpression and/or dysfunction of TRB1/TRB3, mammalian orthologues of Drosophila Tribbles, which regulates differentiation and development, is supposed to participate in the oncogenesis, and they possess characteristics of oncogene. However the precise molecular mechanism remains poorly understood. In this study, we evaluated this hypothesis.
We demonstrated that TRB1 inhibited the transcriptional activity of typical tumor suppressor genes, p53 and FOXO1, to accelerate the proliferation of tumor cells. TRB1 is also one of the proteins responsible for the maintenance of cancer stem cell characters, and the induction of the epidermal-mesenchymal transition (EMT) to activate the invasion and metastasis of cancers, and to acquire the resistance against several anticancer drugs. These results suggested that TRB1 fully participated in the oncogenesis and malignant progression.

Free Research Field

生化学、細胞生物学、腫瘍学

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Published: 2019-03-29  

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