• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to previous page

Functional analysis of BIG3 on triple-negative breast cancer progression

Research Project

Project/Area Number 16K19052
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Pathological medical chemistry
Research InstitutionKindai University (2017)
The University of Tokushima (2016)

Principal Investigator

KIMURA Ryuichiro  近畿大学, 医学部, 助教 (20587323)

Project Period (FY) 2016-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Keywords乳癌 / ゲノム / シグナル伝達 / プロテオーム / 発現制御 / 癌 / 蛋白質
Outline of Final Research Achievements

We identified novel BIG3-interacting factors including microtubule-regulated molecule in ER-negative breast cancer. We further analyzed BIG3-these factors interactions and colocalization by immunoprecipitation and immunostaining. On the other hand, knockdown of BIG3 expression with small-interfering RNA reduced E2F1 expression and cellular growth of ER-negative breast cancer. These results suggest that BIG3 directly regulates cellular survival and growth of ER-negative breast cancer through regulation of microtubule or cell cycle.

Report

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

    (7 results)

All 2018 2017 2016 Other

All Journal Article (1 results) (of which Peer Reviewed: 1 results,  Open Access: 1 results) Presentation (5 results) Remarks (1 results)

  • [Journal Article] Frequent downregulation of LRRC26 by epigenetic alterations is involved in the malignant progression of triple-negative breast cancer2018

    • Author(s)
      Miyagawa Yoshimasa、Matsushita Yosuke、Suzuki Hiromu、Komatsu Masato、Yoshimaru Tetsuro、Kimura Ryuichiro、Yanai Ayako、Honda Junko、Tangoku Akira、Sasa Mitsunori、Miyoshi Yasuo、Katagiri Toyomasa
    • Journal Title

      International Journal of Oncology

      Volume: - Pages: 4301-4301

    • DOI

      10.3892/ijo.2018.4301

    • Related Report
      2017 Annual Research Report
    • Peer Reviewed / Open Access
  • [Presentation] ムチン型糖転移酵素GALNT6はLGALS3BPの糖鎖修飾を通じて乳癌発症を制御する。2017

    • Author(s)
      木村竜一朗、松尾泰佑、尾野雅哉、吉丸哲郎、小松正人、本田純子、朴在賢、中村祐輔、笹三徳、三好康雄、片桐豊雅
    • Organizer
      第76回日本癌学会学術総会(横浜)
    • Related Report
      2017 Annual Research Report
  • [Presentation] トリプルネガティブ乳がんの悪性化におけるRHBDL2の役割解析2017

    • Author(s)
      奥村和正、松下洋輔、小松正人、木村竜一朗、吉丸哲郎、尾野雅哉、三好康雄、本田純子、笹三徳、丹黒章、片桐豊雅
    • Organizer
      第76回日本癌学会学術総会(横浜)
    • Related Report
      2017 Annual Research Report
  • [Presentation] 糖転移酵素GALNT6はガレクチン結合タンパク質1を糖鎖修飾し,乳癌発症を制御する2016

    • Author(s)
      木村竜一朗, 尾野雅哉, 松尾泰佑, 吉丸哲郎, 三好康雄, 笹三徳, 片桐豊雅
    • Organizer
      第75回日本癌学会学術総会
    • Place of Presentation
      パシフィコ横浜(神奈川県横浜市)
    • Year and Date
      2016-10-06
    • Related Report
      2016 Research-status Report
  • [Presentation] トリプルネガティブ乳癌で高発現が認められるTNRHP1の発現亢進は癌の悪性度と相関する2016

    • Author(s)
      奥村和正, 小松正人, 木村竜一朗, 尾野雅哉, 吉丸哲郎, 松下洋輔, 三好康雄, 本田純子, 笹三徳, 丹黒章, 片桐豊雅
    • Organizer
      第75回日本癌学会学術総会
    • Place of Presentation
      パシフィコ横浜(神奈川県横浜市)
    • Year and Date
      2016-10-06
    • Related Report
      2016 Research-status Report
  • [Presentation] BIG3-PHB2相互作用を標的とした前立腺がん治療法の開発の可能性2016

    • Author(s)
      瀧亮祐, 吉丸哲郎, 大豆本圭, 松下洋輔, 木村竜一朗, 尾野雅哉, 片桐豊雅
    • Organizer
      第75回日本癌学会学術総会
    • Place of Presentation
      パシフィコ横浜(神奈川県横浜市)
    • Year and Date
      2016-10-06
    • Related Report
      2016 Research-status Report
  • [Remarks] 徳島大学・教育研究者総覧(木村竜一朗)

    • URL

      http://pub2.db.tokushima-u.ac.jp/ERD/person/277280/work-ja.html

    • Related Report
      2016 Research-status Report

URL: 

Published: 2016-04-21   Modified: 2020-01-20  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi