| Project/Area Number |
26462033
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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 |
Digestive surgery
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| Research Institution | Chiba Cancer Center (Research Institute) |
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Principal Investigator |
Souda Hiroaki 千葉県がんセンター(研究所), 消化器外科, 主任医長 (90261940)
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| Co-Investigator(Kenkyū-buntansha) |
下里 修 千葉県がんセンター(研究所), 発がん研究グループ DNA損傷シグナル研究室, 上席研究員 (30344063)
上條 岳彦 埼玉県立がんセンター(臨床腫瘍研究所), 臨床腫瘍研究所, 研究所長 (90262708)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 大腸癌 / 癌性幹細胞 / CD133 / PTPRK |
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| Outline of Final Research Achievements |
As a higher expression of receptor-type protein tyrosine phosphatase (PTPRK) is considered to be a good prognostic factor for the CD133-expressing colon cancer patients, we sought to investigate the functional significance of the PTPRK-CD133 regulatory axis in the malignant properties of colon cancer cells. Based on our present observations, forced expression of CD133 enhanced a xenograft tumor growth of colon cancer cells and knockdown of PTPRK further promoted the CD133-induced tumor formation in vivo. PTPRK is directly implicated in the dephosphorylation of CD133 in human colon cancer cells. Additionally, PTPRK-depletion dramatically stimulated an anti-apoptotic function of Bad through the activation of the oncogenic CD133-AKT pathway, and thereby significantly reduced an anti-tumor drug-induced cell death. Together, our present observations strongly suggest that the PTPRK-CD133 regulatory axis plays a pivotal role in the regulation of colon cancer progression and drug resistance.
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