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长链非编码RNA HOTAIR通过靶向miR-130a-3p/Suv39H1轴促进乳腺癌细胞的增殖和侵袭/转移。

LncRNA HOTAIR promotes the proliferation and invasion/metastasis of breast cancer cells by targeting the miR-130a-3p/Suv39H1 axis.

作者信息

He Wenxing, Li Dongmei, Zhang Xiaofang

机构信息

Breast Cancer Center,Jiangxi Cancer Hospital of Nanchang University;Jiangxi Key Laboratory of Translational Research for Cancer,No. 519 East Beijing Road, Nanchang, Jiangxi, 330029, China.

出版信息

Biochem Biophys Rep. 2022 May 18;30:101279. doi: 10.1016/j.bbrep.2022.101279. eCollection 2022 Jul.

DOI:10.1016/j.bbrep.2022.101279
PMID:35619625
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9126846/
Abstract

Long noncoding RNAs (lncRNAs) are a group of transcripts, more than 200 bp in size and regulate cell proliferation, differentiation and apoptosis. LncRNA HOX Transcript Antisense Intergenic RNA (HOTAIR) promotes tumor progression and increases cancer susceptibility by regulating microRNA expression and function. HOTAIR regulates miR-130a-3p expression in hepatocellular carcinoma cells. Bioinformatics analysis revealed that Suv39H1 contained a putative binding site for miR-130a-3p. We speculate that LncRNA HOTAIR promotes the proliferation and invasion/metastasis of breast cancer (BC) cells by targeting the miR-130a-3p/Suv39H1 axis. High HOTAIR expression facilitated BC cell growth and metastasis. HOTAIR functioned as a ceRNA by sponging miR-130a-3p and subsequently promoted Suv39H1-mediated AKT/mTOR signaling. Suv39H1 restoration abolished the effects of HOTAIR knockdown on BC cell growth and metastasis. HOTAIR facilitated the Suv39H1-mediated AKT/mTOR pathway by acting as a molecular sponge of miR-130a-3p.Our results provide a better understanding of the interactions of HOTAIR and miR-103a-3p/Suv39H1 in BC and a potential prognostic biomarker and therapeutic target for BC.

摘要

长链非编码RNA(lncRNAs)是一组长度超过200bp的转录本,可调节细胞增殖、分化和凋亡。LncRNA HOX转录反义基因间RNA(HOTAIR)通过调节微小RNA的表达和功能促进肿瘤进展并增加癌症易感性。HOTAIR调节肝癌细胞中miR-130a-3p的表达。生物信息学分析显示,Suv39H1含有miR-130a-3p的假定结合位点。我们推测LncRNA HOTAIR通过靶向miR-130a-3p/Suv39H1轴促进乳腺癌(BC)细胞的增殖和侵袭/转移。HOTAIR高表达促进BC细胞生长和转移。HOTAIR通过海绵吸附miR-130a-3p发挥竞争性内源RNA(ceRNA)的作用,进而促进Suv39H1介导的AKT/mTOR信号传导。恢复Suv39H1可消除HOTAIR敲低对BC细胞生长和转移的影响。HOTAIR通过充当miR-130a-3p的分子海绵促进Suv39H1介导的AKT/mTOR通路。我们的研究结果有助于更好地理解HOTAIR与miR-103a-3p/Suv39H1在BC中的相互作用,并为BC提供了一种潜在的预后生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/27359349d727/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/14c2f10c9ef1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/683c5ce27c99/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/d8321fd336ac/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/f03f44f62cd9/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/226561a77df3/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/27359349d727/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/14c2f10c9ef1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/683c5ce27c99/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/d8321fd336ac/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/f03f44f62cd9/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/226561a77df3/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95c4/9126846/27359349d727/gr6.jpg

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