Bta-miR-106b Regulates Bovine Mammary Epithelial Cell Proliferation, Cell Cycle, and Milk Protein Synthesis by Targeting the CDKN1A Gene

被引:6
|
作者
Wu, Xin [1 ]
Huang, Jinfeng [1 ]
Liu, Yanan [1 ]
Li, Houcheng [1 ]
Han, Bo [1 ]
Sun, Dongxiao [1 ]
机构
[1] China Agr Univ, Coll Anim Sci & Technol, Dept Anim Genet & Breeding, Key Lab Anim Genet, Beijing 100193, Peoples R China
基金
中国国家自然科学基金;
关键词
bta-miR-106b; CDKN1A; BMECs; cell proliferation; milk protein synthesis; MAMMALIAN TARGET; ADIPOSE-TISSUE; MICRORNAS; KINASE; APOPTOSIS; INHIBITION; BIOGENESIS; INITIATION; LACTATION; PI3K/AKT;
D O I
10.3390/genes13122308
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Our previous studies found that bta-miR-106b and its corresponding target gene, CDKN1A, were differentially expressed between the mammary epithelium of lactating Holstein cows with extremely high and low milk protein and fat percentage, implying the potential role of bta-miR-106b in milk composition synthesis. In this study, with luciferase assay experiment, bta-miR-106b was validated to target the 3 '-untranslated region (UTR) of bovine CDKN1A, thereby regulating its expression. Moreover, in bovine mammary epithelial cells (BMECs), over-expression of bta-miR-106b significantly down-regulated the CDKN1A expression at both mRNA and protein levels, and inhibitors of bta-miR-106b increased CDKN1A expression. Of note, we observed that bta-miR-106b accelerated cell proliferation and cell cycle, and changed the expressions of protein synthesis related pathways such as JAK-STAT and PI3K/AKT/mTOR through regulating CDKN1A expression. Our findings highlight the important regulatory role of bta-miR-106b in milk protein synthesis by targeting CDKN1A in dairy cattle.
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页数:14
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