| Project/Area Number |
20591936
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Tohoku University |
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Principal Investigator |
UTSUNOMIYA HIROKI Tohoku University, 大学院・医学系・研究科, 講師 (10359507)
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| Co-Investigator(Kenkyū-buntansha) |
TAKANO Tadao 東北大学, 未来医工学治療開発センター, 准教授 (40282058)
YAEGASHI Nobuo 東北大学, 大学院・医学系研究科, 教授 (00241597)
KOBAYASHI Rika 東北大学, 病院, 技能補佐員 (80451582)
YAMAZAKI Miyuki 東北大学, 病院, 技能補佐員 (90451583)
TAKABAYASHI Toshifumi 東北大学, 医学部, 教授 (30124598)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | Estrogen receptor / 子宮内膜癌 / クロマチン免疫沈降 / GRIP1 / Estroen recetor / エストロゲン受容体 / Erα / クロマチン免疫沈降(ChIP)クローニング / エストロゲン / Glutamate receptor interacting protein 1 (GR1P1) |
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| Research Abstract |
Significant progress has been made in understanding the role of ERα as a transcription factor that regulates the expression of target genes by directly binding to an estrogen response element or by association with other transcription factors on promoter targets. Until recently, however, little had been known about the distribution of ERα-binding sites within the genome and the identity of genes regulated by these cis-acting elements. Our aims were to determine the nature of ERα binding relative to the structure of a gene and increase our understanding of ERα action in Ishikawa endometrial cancer cell line.
Here, we used ChIP cloning technique and identified 47 ERα target loci in Ishikawa cells. The great majority of the binding sites were located in either introns or far distant to coding regions of genes. Among estradiol-induced genes, GRIP1 was found to increase cell survival by significantly reducing apoptosis in Ishikawa cells.
Our findings suggest that at least a subset of these genes may play important biological roles in endometrial cancer.
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