| Project/Area Number |
26460456
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
NAGASHIMA Yoji 東京女子医科大学, 医学部, 教授 (10217995)
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| Co-Investigator(Kenkyū-buntansha) |
秋本 和憲 東京理科大学, 薬学部生命創薬科学科, 准教授 (70285104)
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| Co-Investigator(Renkei-kenkyūsha) |
UEMURA Hiroji (ICHIKAWA Yasushi) 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)
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)
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| 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
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | aPKCλ/ι / 子宮頸癌 / CIN / 前立腺癌 / 腫瘍化 / 乳癌 / GLOI / Cancer / Immunohistochemistry / aPKC / 細胞極性 / 免疫組織化学 / HPV / LST |
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| 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.
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