Deleting maternal Gtl2 leads to growth enhancement and decreased expression of stem cell markers in teratoma
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- TAKAHASHI Nozomi
- Department of Bioscience, Tokyo University of Agriculture, Tokyo 156-0054, Japan
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- YAMAGUCHI Eito
- Department of Bioscience, Tokyo University of Agriculture, Tokyo 156-0054, Japan
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- KAWABATA Yukiko
- Department of Bioscience, Tokyo University of Agriculture, Tokyo 156-0054, Japan
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- KONO Tomohiro
- Department of Bioscience, Tokyo University of Agriculture, Tokyo 156-0054, Japan
書誌事項
- タイトル別名
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- Deleting maternal <i>Gtl2</i> leads to growth enhancement and decreased expression of stem cell markers in teratoma
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抄録
The distal region of mouse chromosome 12 harbors the Dlk1–Dio3 domain, is essential for normal development and encodes maternally expressed noncoding RNAs (ncRNAs), including Gtl2 as well as paternally expressed proteins.Gtl2 works as a tumor suppressor in several types of human cancer cell lines; however, whether this reflects its function in vivo is unknown. Deleting Gtl2 from the maternal allele (Gtl2(–/+)) results in loss of expression of Gtl2 and decreased expression of downstream ncRNAs, including many miRNAs. To determine the role of ncRNAs in tumorigenesis, we induced teratomas by engrafting E6.5 embryos (wildtype or Gtl2(–/+)) under the kidney capsule of scid mice. Some teratomas derived from the Gtl2(–/+) embryos exhibited hypertrophic growth, suggesting that ncRNAs, including Gtl2, may act as tumor suppressors in vivo. Microarray analysis of miRNAs expressed by Gtl2(–/+) teratomas revealed decreased expression of 28 miRNAs encoded by the Dlk1–Dio3 domain, low expression of embryonic stem cell-specific miRNAs and dysregulation of miRNAs involved in tumorigenesis. This study suggests that downregulation of ncRNAs in the Dlk1-Dio3 domain leads to enhanced teratoma growth and repression of stem cell markers.
収録刊行物
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- Journal of Reproduction and Development
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Journal of Reproduction and Development 61 (1), 7-12, 2015
公益社団法人 日本繁殖生物学会
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詳細情報 詳細情報について
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- CRID
- 1390282681314987008
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- NII論文ID
- 130004701540
- 40020374197
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- NII書誌ID
- AA10936678
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- ISSN
- 13484400
- 09168818
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- NDL書誌ID
- 026185979
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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