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Possible regulation of bone resorption in gingival cancer by NKG2D ligands

Research Project

Project/Area Number 16K20612
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Surgical dentistry
Research InstitutionSaitama Medical University

Principal Investigator

Iwasaki Yoshie  埼玉医科大学, 医学部, 助教 (30750880)

Project Period (FY) 2016-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
KeywordsMICA / RANKL / 歯肉癌 / 歯肉癌上皮細胞 / MICA遺伝子 / NKG2Dリガンド / NKG2D / MICA/MICB / NK細胞/T細胞
Outline of Final Research Achievements

Physiologically, in bone remodeling, the source of RANKL is osteoblast and osteocyte. However, we hypothesized that RANKL expression derived from gingival epithelial carcinoma cells may be increased in gingival cancer. As a result, overexpression of MICA in gingival epithelial carcinoma cells induced RANKL expression and the supernatant of these cells promoted osteoclastogenesis.

Report

(3 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report

URL: 

Published: 2016-04-21   Modified: 2019-03-29  

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