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2016 Fiscal Year Final Research Report

Role of aPKC-IL6 pathway, especially in prostatic and berast cancers

Research Project

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Project/Area Number 26460456
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Human pathology
Research InstitutionTokyo Women's Medical University

Principal Investigator

NAGASHIMA Yoji  東京女子医科大学, 医学部, 教授 (10217995)

Co-Investigator(Renkei-kenkyūsha) UEMURA Hiroji  横浜市立大学, 附属病院, 教授 (70254208)
ISHIGURO Hitoshi  横浜市立大学, 医学部, 客員准教授 (00381666)
NAKAIGAWA Noboru  横浜市立大学, 大学院医学研究科, 准教授 (00237207)
ICHIKAWA Yasushi  横浜市立大学, 大学院医学研究科, 教授 (70254208)
AOKI Ichiro  横浜市立大学, 大学院医学研究科, 教授 (00184028)
OHASHI Ken-ichi  横浜市立大学, 大学院医学研究科, 教授 (40231203)
Research Collaborator IZUMISAWA Yuhsuke  横浜市立大学, 大学院生
MIZUSHIMA Taichi  横浜市立大学, 大学院生
KAWASHIMA Masato  横浜市立大学, 技術吏員
Project Period (FY) 2014-04-01 – 2017-03-31
KeywordsaPKCλ/ι / 子宮頸癌 / CIN / 前立腺癌 / 腫瘍化 / 乳癌 / GLOI
Outline of Final Research Achievements

Although aPKClambda/iota (aPKC)is a cell polarity-regulating factor, it has been known to be highly expressed in various cancer cells. We aimed to elucidates the roles of aPKC in development and progression of cancers. In this research, we demonstrated the facts as follows; 1) aPKC is highly expressed in uterine cervical cancer and its precursor, cervical intraepithelial neoplasia (CIN). Additionally, aPKC shows nuclear accumulation along with progression. 2) Cultured normal prostatic cells showed increased proliferation and motility, when aPKC gene is transfected, demonstrating that aPKC has a role in early stage of prostatic carcinogenesis. 3) Breast cancers coexpressiong aPKC, its binding protein p62 and glyoxalase I (GLOI) shows more unfavorable. Combined treatment of inhibitors of aPKC and GLOI effectively suppressed growth of co-expressing breast cancer cells in vitro. These indicated relationship between aPKC signaling and glucose metabolism in breast cancer.

Free Research Field

人体病理学

URL: 

Published: 2018-03-22  

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