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2019 Fiscal Year Final Research Report

Role and regulatory mechanisms of Semaphorin 4D in bone invasion of oral cancer.

Research Project

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Project/Area Number 17K11836
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Surgical dentistry
Research InstitutionOkayama University

Principal Investigator

Ibaragi Soichiro  岡山大学, 医歯薬学総合研究科, 准教授 (80549866)

Co-Investigator(Kenkyū-buntansha) 佐々木 朗  岡山大学, 医歯薬学総合研究科, 教授 (00170663)
Project Period (FY) 2017-04-01 – 2020-03-31
KeywordsSemaphorin 4D / 口腔癌骨浸潤
Outline of Final Research Achievements

In the bone microenvironment, axon guidance molecule Semaphorin 4D (Sema4D) that was secreted by osteoclasts, suppressed bone formation. Sema4D was also identified in many cancer cells and plays a role in tumor growth. This research demonstrated the role of Sema4D in bone invasion of oral cancer.
Sema4D that was produced by oral cancer cells, increased cancer cell activity in an autocrine manner. Sema4D also regulated the expression of RANKL in osteoblasts, and which stimulated osteoclastgenesis and bone invasion of oral cancer cells. IGF-I that was released from destructed bone tissue, regulated Sema4D expression and increased further tumor growth and bone invasion.

Free Research Field

口腔外科

Academic Significance and Societal Importance of the Research Achievements

本研究は,口腔癌細胞の産生するSema4Dが口腔癌細胞の増殖と破骨細胞形成を促進し,骨浸潤を促進していることを明らかにした.さらに口腔癌細胞のSema4D発現を制御しているのは,破壊された骨組織から遊離されたIGF-Iであることを突き止めた.本研究を発展させ抗Sema4D 療法が臨床応用できれば,癌細胞および破骨細胞の両方を標的とした新規治療法の候補となると考えられた.

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Published: 2021-02-19  

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