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长链非编码RNA EIF3J-AS1通过调控MAFG发挥癌基因作用,促进前列腺癌进展。

LncRNA EIF3J-AS1 functions as an oncogene by regulating MAFG to promote prostate cancer progression.

作者信息

Ye Chen, Qin Shengfei, Guo Fei, Yang Yue, Wang Huiqing, Zhang Chao, Yang Bo

机构信息

Department of Urology, Shanghai Changhai Hospital, P. R. China, Shanghai 200433, China.

出版信息

J Cancer. 2022 Jan 1;13(1):146-152. doi: 10.7150/jca.60676. eCollection 2022.

DOI:10.7150/jca.60676
PMID:34976178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8692703/
Abstract

Long non-coding RNAs (lncRNAs) can modulate various biological processes and behaviors in most human cancers. LncRNA EIF3J-AS1 has been reported as an oncogene in various tumors, but whether it exerts functions in malignant progression and gene expression in prostate cancer (PCa) remains unknown. In this study, we investigated the high level of EIF3J-AS1 in PCa tissues and cells, and used functional assays to show that knocking down EIF3J-AS1 inhibited PCa cell proliferation and metastatic ability. A preliminary mechanistic investigation also showed that EIF3J-AS1 may increase the expression of MAF bZIP transcription Factor G (MAFG) in PCa. The expression correlation between EIF3J-AS1 and MAFG was found to be positive in PCa tissues. Finally, rescue assays showed that MAFG might be involved in the EIF3J-AS1-mediated malignant phenotype in PCa cells. This study demonstrated that EIF3J-AS1/MAFG may play a key role in facilitating PCa progression.

摘要

长链非编码RNA(lncRNAs)可调节大多数人类癌症中的各种生物学过程和行为。lncRNA EIF3J-AS1在多种肿瘤中被报道为致癌基因,但它是否在前列腺癌(PCa)的恶性进展和基因表达中发挥作用仍不清楚。在本研究中,我们调查了PCa组织和细胞中EIF3J-AS1的高表达水平,并通过功能实验表明敲低EIF3J-AS1可抑制PCa细胞增殖和转移能力。一项初步的机制研究还表明,EIF3J-AS1可能增加PCa中MAF bZIP转录因子G(MAFG)的表达。在PCa组织中发现EIF3J-AS1与MAFG之间存在正表达相关性。最后,挽救实验表明MAFG可能参与了EIF3J-AS1介导的PCa细胞恶性表型。本研究表明,EIF3J-AS1/MAFG可能在促进PCa进展中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/a8a056fbc377/jcav13p0146g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/bdfc73ba7450/jcav13p0146g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/4729e96a3d14/jcav13p0146g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/a8a056fbc377/jcav13p0146g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/bdfc73ba7450/jcav13p0146g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/7ea63da8c61d/jcav13p0146g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/bc2bf906d32c/jcav13p0146g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/4729e96a3d14/jcav13p0146g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e830/8692703/a8a056fbc377/jcav13p0146g005.jpg

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Nat Rev Mol Cell Biol. 2021 Feb;22(2):96-118. doi: 10.1038/s41580-020-00315-9. Epub 2020 Dec 22.
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EIF3J-AS1 promotes glioma cell growth via up-regulating ANXA11 through sponging miR-1343-3p.
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Sci Rep. 2020 Aug 18;10(1):13969. doi: 10.1038/s41598-020-70886-2.
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