Regulatory mechanism of tumor cell proliferation by pluripotency-associated transcriptional repressor NACC1
Project/Area Number |
24790391
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Experimental pathology
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Research Institution | Iwate Medical University |
Principal Investigator |
KASAI Shuya 岩手医科大学, 医学部, 研究員 (20609664)
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Project Status |
Completed (Fiscal Year 2013)
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Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | NACC1 / 乳癌 / 腫瘍増殖 / 腫瘍悪性化 |
Research Abstract |
Elevated expression of NACC1 associates with tumor recurrence and growth of breast, ovarian and cervical cancers. To clarify the molecular mechanism of tumor growth acceleration by NACC1 overexpression in human malignancies, we determined whether NACC1 regulates beta-catenin/TCF pathway in breast cancer cell lines. In parallel, proteomic analysis of NACC1 interacting proteins was carried out. We identified NACC2, ZKSCAN1 and PLK1 as novel NACC1-intracting proteins. NACC1-PLK1 interaction was elevated in cells synchronized at metaphase compared to asynchronous cells. PLK1 expression and NACC1-PLK1 colocalization was observed specifically in metaphase, whereas NACC1 expression was observed in any cell cycle stages. In addition, NACC1 phosphorylation by PLK1 was elevated by metaphase synchronization.
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Report
(3 results)
Research Products
(7 results)
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[Journal Article] Transcriptional and post-transcriptional regulation of βIII-tubulin protein expression in relation with cell cycle-dependent regulation of tumor cells2012
Author(s)
Shibazaki M, Maesawa C, Akasaka K, Kasai S, Yasuhira S, Kanno K, Nakayama I, Sugiyama T, Wakabayasi G, Masuda T, Mori N
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Journal Title
Int.J.Oncol.
Volume: 40(3)
Pages: 695-702
DOI
Related Report
Peer Reviewed
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