Identification of novel EZH2 mechanism and its network in cancer cells
| Project/Area Number |
26430136
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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 |
Tumor biology
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| Research Institution | Nagoya City University |
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Principal Investigator |
SHINJO Keiko 名古屋市立大学, 大学院医学研究科, 助教 (40641618)
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| Co-Investigator(Renkei-kenkyūsha) |
KONDO Yutaka 名古屋市立大学, 大学院医学研究科, 教授 (00419897)
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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 |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | EZH2 / IKBKE / がん / リン酸化 |
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| Outline of Final Research Achievements |
Enhancer of zeste homologue 2 (EZH2) is overexpressed in many types of cancer and associated with poor prognosis. However, the underlying mechanism of EZH2 overexpression is not fully understood. Using an EZH2 promoter inhibition assay with an siRNA library targeting known human kinases in colorectal cancer cell lines, we identified a novel role for the IKBKE－NF-κB pathway in upregulating EZH2 expression. IKKe a kinase, was observed to be highly expressed in colorectal cancer tissue. Further validation revealed that inhibiting IKBKE caused a significant reduction in EZH2 expression. These data suggest that the IKKe;－NF-κB pathway may play an important role in regulation of EZH2 expression in colorectal cancer.
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Report
(4 results)
Research Products
(22 results)
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[Journal Article] Targeting the Notch-regulated non-coding RNA TUG1 for glioma treatment.2016
Author(s)
Katsushima K, Natsume A, Ohka F, Shinjo K, Hatanaka A, Ichimura N, Sato S, Takahashi S, Kimura H, Totoki Y, Shibata T, Naito M, Kim HJ, Miyata K, Kataoka K, Kondo Y.
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Journal Title
Nat Commun.
Volume: 7
Issue: 1
Pages: 13616-13616
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Aberrant TET1 Methylation Closely Associated with CpG Island Methylator Phenotype in Colorectal Cancer.2015
Author(s)
5.Ichimura N, Shinjo K, An B, Shimizu Y, Yamao K, Ohka F, Katsushima K, Hatanaka A, Tojo M, Yamamoto E, Suzuki H, Ueda M, Kondo Y
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Journal Title
Cancer Prev Res (Phila)
Volume: 10
Issue: 8
Pages: 702-11
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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[Journal Article] Long-Term Pancreatic Beta Cell Exposure to High Levels of Glucose but Not Palmitate Induces DNA Methylation within the Insulin Gene Promoter and Represses Transcriptional Activity.2015
Author(s)
Ishikawa K, Tsunekawa S, Ikeniwa M, Izumoto T, Iida A, Ogata H, Uenishi E, Seino Y, Ozaki N, Sugimura Y, Hamada Y, Kuroda A, Shinjo K, Kondo Y, Oiso Y.
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Journal Title
PLoS One
Volume: 10(2)
Issue: 2
Pages: e0115350-e0115350
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] miR-615-5p is epigenetically inactivated and functions as a tumor suppressor in pancreatic ductal adenocarcinoma.2015
Author(s)
Gao W, Gu Y, Li Z, Cai H, Peng Q, Tu M, Kondo Y, Shinjo K, Zhu Y, Zhang J, Sekido Y, Han B, Qian Z, Miao Y.
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Journal Title
Oncogene
Volume: 34
Issue: 13
Pages: 1629-40
DOI
Related Report
Peer Reviewed
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