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环状FLT1和lncCCPG1通过促进lncSLC30A9表达来海绵化miR-93,从而调节脂肪细胞的增殖和分化。

circFLT1 and lncCCPG1 Sponges miR-93 to Regulate the Proliferation and Differentiation of Adipocytes by Promoting lncSLC30A9 Expression.

作者信息

Kang Zihong, Zhang Sihuang, Jiang Enhui, Wang Xinyu, Wang Zhen, Chen Hong, Lan Xianyong

机构信息

College of Animal Science and Technology, Northwest A&F University, Yangling Shaanxi 712100, China.

出版信息

Mol Ther Nucleic Acids. 2020 Sep 16;22:484-499. doi: 10.1016/j.omtn.2020.09.011. eCollection 2020 Dec 4.

DOI:10.1016/j.omtn.2020.09.011
PMID:33230451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7554329/
Abstract

Although many circular RNAs (circRNAs) and long non-coding RNAs (lncRNAs) have been discovered in adipocytes, their precise functions and molecular mechanisms remain poorly understood. Based on existing circRNA and lncRNA sequencing data of bovine adipocytes, we screened for the differential expression of and in preadipocytes and adipocytes and further analyzed their function and regulation during adipogenesis. The overexpression of and together facilitated adipocyte differentiation and suppressed proliferation. Computationally, the RNA hybrid showed that and had multiple potential binding sites with miR-93. Additionally, luciferase reporting experiments verified that and may interact with miR-93. We also demonstrated that overexpressed miR-93 effectively suppresses the expression of . Signaling pathway enrichment analysis, luciferase activity assay, and expression analysis revealed that inhibits proliferation by inhibiting the expression of AKT protein and promotes differentiation by recruiting the FOS protein to the promoter of peroxisome proliferator-activated receptor gamma (). In sum, our results elucidate the regulatory mechanisms of and as miR-93 sponges in bovine adipocytes.

摘要

尽管在脂肪细胞中已发现许多环状RNA(circRNA)和长链非编码RNA(lncRNA),但其确切功能和分子机制仍知之甚少。基于现有的牛脂肪细胞circRNA和lncRNA测序数据,我们筛选了前脂肪细胞和脂肪细胞中[具体名称未给出]的差异表达,并进一步分析了它们在脂肪生成过程中的功能和调控。[具体名称未给出]的共同过表达促进了脂肪细胞分化并抑制了增殖。通过计算,RNA杂交显示[具体名称未给出]与miR-93有多个潜在结合位点。此外,荧光素酶报告实验证实[具体名称未给出]可能与miR-93相互作用。我们还证明,过表达的miR-93有效抑制了[具体名称未给出]的表达。信号通路富集分析、荧光素酶活性测定和表达分析表明,[具体名称未给出]通过抑制AKT蛋白的表达来抑制增殖,并通过将FOS蛋白招募到过氧化物酶体增殖物激活受体γ(PPARγ)的启动子来促进分化。总之,我们的结果阐明了[具体名称未给出]作为牛脂肪细胞中miR-93海绵的调控机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/eadf9c8e6480/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/8c9c7e735765/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/d82a4d324c87/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/10b97bcde444/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/2597a455c8a1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/75229213bda7/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/9f76d2366401/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/00ddaa5f9222/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/850071100d51/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/b969d9ec44f3/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/eadf9c8e6480/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/8c9c7e735765/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/d82a4d324c87/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/10b97bcde444/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/2597a455c8a1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/75229213bda7/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/9f76d2366401/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/00ddaa5f9222/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/850071100d51/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/b969d9ec44f3/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/672b/7554329/eadf9c8e6480/gr9.jpg

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