The roles of SATB2 and NGR1 genes which were extracted as candidates for upstream regulatory factors involved in the pathogenesis of uterine leiomyomas
Project/Area Number |
15K10720
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Obstetrics and gynecology
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Research Institution | Yamaguchi University |
Principal Investigator |
SATO Shun 山口大学, 大学院医学系研究科, 助教 (10534604)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Project Status |
Completed (Fiscal Year 2017)
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Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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Keywords | 子宮筋腫 / DNAメチル化 / マスター遺伝子 / 遺伝子発現 / 異種移植 |
Outline of Final Research Achievements |
We extracted SATB2 and NRG1 genes as candidates for upstream regulatory genes based on a hypothesis that the aberrant expression of upstream regulatory genes caused by aberrant DNA methylation is associated with the pathogenesis of uterine leiomyomas. To infer the functions of the genes, cell lines overexpressing each gene were established and their transcriptome and pathway analyses were performed. WNT/β-catenin and TGF-β signaling related to the pathogenesis of leiomyomas were activated by both SATB2 and NRG1 overexpression. The signaling of growth factors including VEGF, PDGF and IGF1, and the retinoic acid signaling, which are associated with the growth of leiomyomas, were activated in SATB2 and NRG1 overexpression, respectively. The results indicate that SATB2 and NRG1 overexpression induced most of the signaling pathways that are currently considered to be involved in the pathogenesis of leiomyomas, suggesting that these genes have roles as the upstream regulatory factors.
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Report
(4 results)
Research Products
(36 results)
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[Journal Article] Thin endometrium transcriptome analysis reveals a potential mechanism of implantation failure2017
Author(s)
Maekawa R, Taketani T, Mihara Y, Sato S, Okada M, Tamura I, Jozaki K, Kajimura T, Asada H, Tamura H, Takasaki A, Sugino N
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Journal Title
Reprod Med Biol
Volume: 16
Issue: 2
Pages: 206-227
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Novel Function of a Transcription Factor WT1 in Regulating Decidualization in Human Endometrial Stromal Cells and Its Molecular Mechanism2017
Author(s)
Tamura I, Shirafuta Y, Jozaki K, Kajimura T, Shinagawa M, Maekawa R, Taketani T, Asada H, Sato S, Tamura H, Sugino N
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Journal Title
Endocrinology
Volume: 158
Issue: 10
Pages: 3696-3707
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Long-term melatonin treatment delays ovarian aging.2017
Author(s)
Tamura H, Kawamoto M, Sato S, Tamura I, Maekawa R, Taketani T, Aasada H, Takaki E, Nakai A, Reiter RJ, Sugino N.
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Journal Title
Journal of Pineal Research
Volume: 印刷中
Issue: 2
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Tissue-Specific Expression of Estrogen Receptor 1 Is Regulated by DNA Methylation in a T-DMR2016
Author(s)
Maekawa R, Sato S, Okada M, Lee L, Tamura I, Jozaki K, Kajimura T, Asada H, Yamagata Y, Tamura H, Yamamoto S, Sugino N
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Journal Title
Mol Endocrinol
Volume: 30
Issue: 3
Pages: 335-47
DOI
NAID
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Retinoic acid has the potential to suppress endometriosis development.2015
Author(s)
Yamagata Y, Takaki E, Shinagawa M, Okada M, Jozaki K, Lee L, Sato S, Maekawa R, Taketani T, Asada H, Tamura H, Nakai A, Sugino N.
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Journal Title
J Ovarian Res.
Volume: 8
Issue: 1
Pages: 49-49
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Presentation] 次世代シークエンサーを用いたヒト子宮内膜間質細胞 (ESC) の脱落膜化に伴いヒストン修飾と発現が上昇した遺伝子群の検討2015
Author(s)
城﨑幸介, 田村功, 品川征大, 岡田真紀, 李理華, 前川亮, 浅田裕美, 佐藤俊, 山縣芳明, 田村博史, 杉野法広
Organizer
第88回日本内分泌学会学術総会
Place of Presentation
東京・ホテルニューオータニ東京
Year and Date
2015-04-23
Related Report
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