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2019 Fiscal Year Final Research Report

Cooperative epithelial cell tumorigenesis by APOBEC3s expressed in the nucleus and cytoplasm induced by EBV infection

Research Project

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Project/Area Number 18K15168
Research Category

Grant-in-Aid for Early-Career Scientists

Allocation TypeMulti-year Fund
Review Section Basic Section 49060:Virology-related
Research InstitutionShimane University

Principal Investigator

Kanehiro Yuichi  島根大学, 学術研究院医学・看護学系, 助教 (60609197)

Project Period (FY) 2018-04-01 – 2020-03-31
KeywordsEBウイルス / APOBEC3 / ミトコンドリア
Outline of Final Research Achievements

We studied the role of the nuclear- and cytoplasm-localized DNA editing enzyme APOBEC3 in the tumorigenesis of EBV-infected epithelial cells.Infection experiments using recombinant EBV-eGFP revealed that EBV infection induces the expression of cytoplasm-localized APOBEC3C via type I IFNs and that mitochondria are injured by mutations in mtDNA by APOBEC3C.Since the nuclear-localized APOBEC3A is also induced by type I IFNs, we hypothesized that cytoplasm-localized and nuclear-localized APOBEC3 induced by EBV infection would introduce mutations into the host and mitochondrial genomes in a coordinated manner, leading to cell tumorigenesis.

Free Research Field

ウイルス学

Academic Significance and Societal Importance of the Research Achievements

EBウイルス陽性上皮細胞性腫瘍は、単一のウイルス感染細胞が腫瘍化したものである。EBV感染がAPOBEC3を介して宿主ゲノムやミトコンドリアゲノムに変異を導入し、細胞を腫瘍化に導くとすれば、APOBEC3は発がんのリスク因子となりうる。従って、EBV感染が誘導するAPOBEC3による腫瘍化機構を明らかにすれば、EBV感染で発生する上皮細胞性腫瘍の予防法が開発できる。また宿主ゲノムやミトコンドリアゲノムへの変異は、多くのウイルス感染に共通の現象である可能性が高く、本研究は多くのウイルス感染による腫瘍の発生にAPOBEC3が関わっている可能性を示すことになる。

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Published: 2021-02-19  

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