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miR-17/92簇是STAT5的作用靶点，但对乳腺发育并非必需。

The miR-17/92 cluster is targeted by STAT5 but dispensable for mammary development.

作者信息

Feuermann Yonatan, Robinson Gertraud W, Zhu Bing-Mei, Kang Keunsoo, Raviv Noa, Yamaji Daisuke, Hennighausen Lothar

机构信息

Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

Genesis. 2012 Sep;50(9):665-71. doi: 10.1002/dvg.22023. Epub 2012 Mar 31.

DOI:10.1002/dvg.22023
PMID:22389215
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3560854/
Abstract

Genome wide analysis revealed the miR-17/92 cluster as a STAT5 target. This cluster encodes six microRNAs, which predictably target genes that play a role in mammary gland development. In this study, we have deleted the miR-17/92 cluster in mammary stem cells and evaluated in the mouse its function during mammary gland development. Loss of the miR-17/92 cluster did not affect mammary development from prepuberty to lactation. Our studies demonstrated that, while expression of the miR-17/92 cluster is under control of the key mammary transcription factor STAT5, its presence is not required for normal mammary development or lactation.

摘要

全基因组分析显示miR-17/92簇是STAT5的一个靶点。该簇编码六种微小RNA，可预测地靶向在乳腺发育中起作用的基因。在本研究中，我们在乳腺干细胞中删除了miR-17/92簇，并在小鼠中评估了其在乳腺发育过程中的功能。miR-17/92簇的缺失并不影响从青春期前到哺乳期的乳腺发育。我们的研究表明，虽然miR-17/92簇的表达受关键乳腺转录因子STAT5的控制，但其存在对于正常的乳腺发育或泌乳并非必需。

相似文献

[1]
The miR-17/92 cluster is targeted by STAT5 but dispensable for mammary development.

Genesis. 2012-9

[2]
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[3]
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[4]
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Mol Endocrinol. 2006-3

[5]
Sequential activation of genetic programs in mouse mammary epithelium during pregnancy depends on STAT5A/B concentration.

Nucleic Acids Res. 2012-12-28

[6]
Conditional deletion of Shp2 in the mammary gland leads to impaired lobulo-alveolar outgrowth and attenuated Stat5 activation.

J Biol Chem. 2006-11-10

[7]
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[8]
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[9]
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[10]
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[2]
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Biol Open. 2024-6-15

[3]
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[4]
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Int J Mol Sci. 2022-12-15

[5]
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[6]
The Wnt/β-Catenin/LEF1 Pathway Promotes Cell Proliferation at Least in Part Through Direct Upregulation of miR-17-92 Cluster.

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[7]
Prognostic value of miR-17-5 p in gastrointestinal cancers: a systematic review and meta-analysis.

Onco Targets Ther. 2018-9-19

[8]
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RNA Biol. 2017-9-29

[9]
Constitutive expression of microRNA-150 in mammary epithelium suppresses secretory activation and impairs de novo lipogenesis.

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[10]
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本文引用的文献

[1]
Genome-wide analyses reveal the extent of opportunistic STAT5 binding that does not yield transcriptional activation of neighboring genes.

Nucleic Acids Res. 2012-2-8

[2]
MicroRNAs MiR-17, MiR-20a, and MiR-106b act in concert to modulate E2F activity on cell cycle arrest during neuronal lineage differentiation of USSC.

PLoS One. 2011-1-20

[3]
The miR-17-92 microRNA cluster regulates multiple components of the TGF-β pathway in neuroblastoma.

Mol Cell. 2010-12-10

[4]
miR-212 and miR-132 are required for epithelial stromal interactions necessary for mouse mammary gland development.

Nat Genet. 2010-11-7

[5]
The myc-miR-17~92 axis blunts TGF{beta} signaling and production of multiple TGF{beta}-dependent antiangiogenic factors.

Cancer Res. 2010-10-12

[6]
Tissue-specific regulation of mouse microRNA genes in endoderm-derived tissues.

Nucleic Acids Res. 2010-9-14

[7]
TGF-beta biology in mammary development and breast cancer.

Cold Spring Harb Perspect Biol. 2011-1-1

[8]
miR-17-92 cluster: ups and downs in cancer and aging.

Biogerontology. 2010-5-1

[9]
Characterisation of microRNA expression in post-natal mouse mammary gland development.

BMC Genomics. 2009-11-20

[10]
Development of mammary luminal progenitor cells is controlled by the transcription factor STAT5A.

Genes Dev. 2009-10-15

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