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Does a tumor-associated antigen, EpCAM, regulate formation and function of tight junction in striated squamous epithelium?

Research Project

Project/Area Number 17H07304
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeSingle-year Grants
Research Field Morphological basic dentistry
Research InstitutionFukuoka Dental College

Principal Investigator

SEO AKIRA  福岡歯科大学, 口腔歯学部, 助教 (70804037)

Research Collaborator Inai Tetsuichiro  , 教授
Kitagawa Norio  
Otani Takahito  
Nikaido Misaki  
Ozaki Akane  
Miyazono Shoji  
Project Period (FY) 2017-08-25 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywordsタイト結合 / EpCAM / ケラチノサイト / 細胞間透過性 / tight junction / claudin / permeability
Outline of Final Research Achievements

In cancer, highly expressed EpCAM is a transmembrane glycoprotein involved in cell adhesion, cell proliferation, and tumor progression, and expression is also observed in stratified squamous epithelium, which is a normal tissue. We aimed to create keratinocytes from which the EpCAM gene has been disrupted and to investigate changes in tight junction formation and intercellular permeability during stratified squamous epithelium formation using a three-dimensional culture system. In this study, a three-dimensional culture method using the mouse keratinocyte strain (K38) formed a non-keratinized stratified squamous epithelium like the oral mucosa epithelium The expression of the tight junction membrane protein claudin (CL) 1, 4, 6, 7 was examined by Western blot and fluorescent immunostaining to confirm that it was almost similar to that of the living body. However, cells in which the EpCAM gene was disrupted could not be obtained.

Academic Significance and Societal Importance of the Research Achievements

本研究では、線維芽細胞を使わずケラチノサイト単独で重層扁平上皮を構築する三次元培養系を用いることで、線維芽細胞からの間接的な影響(成長因子などの分泌蛋白)を排除して、上皮単独で解析できる点で意義がある。また、目的とする遺伝子産物をマウスで破壊して解析する場合、一般的には多大な労力と費用がかかる。さらに、機能的・形態的に明瞭な変化がなかったり、胎生致死であるためにその後の解析が困難な場合があり得る。本研究では、ケラチノサイトで働く遺伝子の機能を解析するためのひとつのスクリーニング系として活用できる点で意義がある。

Report

(3 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Annual Research Report
  • Research Products

    (5 results)

All 2018 2017

All Presentation (5 results)

  • [Presentation] 血清がケラチノサイトの角化,分化およびタイト結合に及ぼす影響についての解析2018

    • Author(s)
      尾崎茜, 北河憲雄, 大谷崇仁, 緒方佳代子, 瀬尾皓, 小島寛, 稲井哲一朗
    • Organizer
      第45回福岡歯科大学学会総会
    • Related Report
      2018 Annual Research Report
  • [Presentation] ストレス応答MAPキナーゼの活性化によるケラチノサイトのタイト結合についての解析2018

    • Author(s)
      二階堂美咲, 北河憲雄, 大谷崇仁, 緒方佳代子, 瀬尾皓, 阿南壽, 稲井哲一朗
    • Organizer
      第45回福岡歯科大学学会総会
    • Related Report
      2018 Annual Research Report
  • [Presentation] マウスケラチノサイトによる非角化および角化重層扁平上皮様構造の形成2017

    • Author(s)
      尾崎 茜,瀬尾 皓,松浦尚志,小島 寛,稲井哲一朗
    • Organizer
      第44回福岡歯科学会総会
    • Related Report
      2017 Annual Research Report
  • [Presentation] マウスケラチノサイトにおけるJNK1の解析2017

    • Author(s)
      二階堂美咲,北河憲雄,大谷崇仁,瀬尾 皓,阿南 壽,稲井哲一朗
    • Organizer
      第44回福岡歯科学会総会
    • Related Report
      2017 Annual Research Report
  • [Presentation] ビタミンA誘導体による角化抑制の解析2017

    • Author(s)
      宮園祥爾,北河憲雄,大谷崇仁,瀬尾皓,松浦尚志,稲井哲一朗
    • Organizer
      第44回福岡歯科学会総会
    • Related Report
      2017 Annual Research Report

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Published: 2017-08-25   Modified: 2020-03-30  

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