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2
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MicroRNA-100 inhibits breast cancer cell proliferation, invasion and migration by targeting FOXA1.微小RNA-100通过靶向叉头框蛋白A1抑制乳腺癌细胞的增殖、侵袭和迁移。
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LncRNA TUG1 promotes cell proliferation and suppresses apoptosis in osteosarcoma by regulating miR-212-3p/FOXA1 axis.长链非编码 RNA TUG1 通过调控 miR-212-3p/FOXA1 轴促进骨肉瘤细胞增殖并抑制凋亡。
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[MicroRNA-30a inhibits proliferation of hepatocellular carcinoma cells via targeted regulation of forkhead-box protein A1].[微小RNA-30a通过靶向调控叉头框蛋白A1抑制肝癌细胞增殖]
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Long noncoding RNA enhances the malignant properties of osteosarcoma by increasing forkhead box A1 expression via sponging of microRNA-483-3p.长链非编码RNA通过海绵吸附微小RNA-483-3p增加叉头框A1的表达,从而增强骨肉瘤的恶性特性。
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microRNA-200a functions as a tumor suppressor by targeting FOXA1 in glioma.微小RNA-200a通过靶向叉头框蛋白A1在胶质瘤中发挥肿瘤抑制作用。
Exp Ther Med. 2019 Jan;17(1):221-229. doi: 10.3892/etm.2018.6895. Epub 2018 Oct 29.
7
Long non-coding RNA TUG1 promotes osteosarcoma cell proliferation and invasion through inhibition of microRNA-212-3p expression.长链非编码RNA TUG1通过抑制微小RNA-212-3p的表达促进骨肉瘤细胞的增殖和侵袭。
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MicroRNA-935 Inhibits Proliferation and Invasion of Osteosarcoma Cells by Directly Targeting High Mobility Group Box 1.微小RNA-935通过直接靶向高迁移率族蛋白盒1抑制骨肉瘤细胞的增殖和侵袭。
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本文引用的文献

1
miR-212/132 downregulates SMAD2 expression to suppress the G1/S phase transition of the cell cycle and the epithelial to mesenchymal transition in cervical cancer cells.微小RNA-212/132下调SMAD2表达,以抑制宫颈癌细胞的细胞周期G1/S期转换和上皮-间质转化。
IUBMB Life. 2015 May;67(5):380-94. doi: 10.1002/iub.1381. Epub 2015 May 19.
2
MicroRNA-212 suppresses tumor growth of human hepatocellular carcinoma by targeting FOXA1.微小RNA-212通过靶向叉头框蛋白A1抑制人肝细胞癌的肿瘤生长。
Oncotarget. 2015 May 30;6(15):13216-28. doi: 10.18632/oncotarget.3916.
3
FOXA1 modulates EAF2 regulation of AR transcriptional activity, cell proliferation, and migration in prostate cancer cells.叉头框蛋白A1(FOXA1)调节EAF2对前列腺癌细胞中雄激素受体(AR)转录活性、细胞增殖和迁移的调控。
Prostate. 2015 Jun 15;75(9):976-87. doi: 10.1002/pros.22982. Epub 2015 Mar 23.
4
FOXA1 positively regulates gene expression by changing gene methylation status in human breast cancer MCF-7 cells.FOXA1 通过改变人乳腺癌 MCF-7 细胞中的基因甲基化状态来正向调控基因表达。
Int J Clin Exp Pathol. 2015 Jan 1;8(1):96-106. eCollection 2015.
5
PI3K/Akt signaling in osteosarcoma.骨肉瘤中的PI3K/Akt信号传导
Clin Chim Acta. 2015 Apr 15;444:182-92. doi: 10.1016/j.cca.2014.12.041. Epub 2015 Feb 19.
6
MicroRNA-212 inhibits osteosarcoma cells proliferation and invasion by down-regulation of Sox4.微小RNA-212通过下调Sox4抑制骨肉瘤细胞的增殖和侵袭。
Cell Physiol Biochem. 2014;34(6):2180-8. doi: 10.1159/000369661. Epub 2014 Dec 2.
7
miR-126 inhibits cell growth, invasion, and migration of osteosarcoma cells by downregulating ADAM-9.微小RNA-126通过下调解聚素和金属蛋白酶9来抑制骨肉瘤细胞的生长、侵袭和迁移。
Tumour Biol. 2014 Dec;35(12):12645-54. doi: 10.1007/s13277-014-2588-3. Epub 2014 Sep 12.
8
MiR-212 exerts suppressive effect on SKOV3 ovarian cancer cells through targeting HBEGF.微小RNA-212通过靶向肝素结合表皮生长因子(HBEGF)对SKOV3卵巢癌细胞发挥抑制作用。
Tumour Biol. 2014 Dec;35(12):12427-34. doi: 10.1007/s13277-014-2560-2. Epub 2014 Sep 9.
9
Blocked autophagy by miR-101 enhances osteosarcoma cell chemosensitivity in vitro.miR-101阻断自噬增强骨肉瘤细胞体外化疗敏感性。
ScientificWorldJournal. 2014;2014:794756. doi: 10.1155/2014/794756. Epub 2014 Jun 9.
10
The tumor suppressor role of miR-124 in osteosarcoma.miR-124在骨肉瘤中的肿瘤抑制作用。
PLoS One. 2014 Jun 27;9(6):e91566. doi: 10.1371/journal.pone.0091566. eCollection 2014.

微小RNA-212通过靶向叉头框蛋白A1抑制骨肉瘤细胞的增殖和迁移。

MicroRNA-212 suppresses the proliferation and migration of osteosarcoma cells by targeting forkhead box protein A1.

作者信息

Liu Jian, Chen Bohua, Yue Bin, Yang Junde

机构信息

Department of Orthopedics, Eighth People's Hospital of Qingdao, Medical School of Qingdao University, Qingdao, Shandong 266100, P.R. China.

出版信息

Exp Ther Med. 2016 Dec;12(6):4135-4141. doi: 10.3892/etm.2016.3880. Epub 2016 Nov 7.

DOI:10.3892/etm.2016.3880
PMID:28101191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5228200/
Abstract

MicroRNAs (miRNAs) are a class of small non-coding RNAs that function as critical gene regulators by targeting the 3' untranslated region (UTR) of mRNA, causing translational repression or mRNA degradation. Deregulation of specific miRNAs, including miR-212, has been identified in patients with osteosarcoma. However, the underlying mechanism is yet to be fully elucidated. The present study aimed to reveal the regulatory mechanism of miR-212 in osteosarcoma cell viability and migration. Quantitative polymerase chain reaction data revealed that miR-212 was significantly downregulated in osteosarcoma tissues compared with normal bone tissues. miR-212 was also downregulated in osteosarcoma cell lines compared with normal osteoblast cell lines. Overexpression of miR-212 significantly suppressed the viability and migration of human osteosarcoma MG-63 and Saos-2 cell lines. In addition, forkhead box protein A1 (FOXA1), an oncogene in osteosarcoma, was predicted to be a putative target of miR-212 by bioinformatical analysis. Furthermore, luciferase reporter assay data confirmed that miR-212 could directly bind to the seed sequences within the 3'UTR of FOXA1 mRNA, and miR-212 negatively mediated the protein levels of FOXA1 in osteosarcoma MG-63 and Saos-2 cells. Moreover, knockdown of FOXA1 also led to a significant decrease in the viability and migration of osteosarcoma MG-63 and Saos-2 cells and the expression levels of FOXA1 were significantly upregulated in osteosarcoma tissues and cell lines. These data suggest that miR-212 inhibits the viability and migration of osteosarcoma cells by targeting FOXA1. Accordingly, miR-212 may become a potential candidate for osteosarcoma therapy.

摘要

微小RNA(miRNA)是一类小的非编码RNA,通过靶向mRNA的3'非翻译区(UTR)发挥关键基因调节作用,导致翻译抑制或mRNA降解。在骨肉瘤患者中已发现特定miRNA(包括miR-212)失调。然而,其潜在机制尚未完全阐明。本研究旨在揭示miR-212在骨肉瘤细胞活力和迁移中的调节机制。定量聚合酶链反应数据显示,与正常骨组织相比,miR-212在骨肉瘤组织中显著下调。与正常成骨细胞系相比,miR-212在骨肉瘤细胞系中也下调。miR-212的过表达显著抑制了人骨肉瘤MG-63和Saos-2细胞系的活力和迁移。此外,通过生物信息学分析预测,骨肉瘤中的癌基因叉头框蛋白A1(FOXA1)是miR-212的假定靶标。此外,荧光素酶报告基因检测数据证实,miR-212可直接结合FOXA1 mRNA 3'UTR内的种子序列,并且miR-212负向调节骨肉瘤MG-63和Saos-2细胞中FOXA1的蛋白水平。此外,敲低FOXA1也导致骨肉瘤MG-63和Saos-2细胞的活力和迁移显著降低,并且FOXA1的表达水平在骨肉瘤组织和细胞系中显著上调。这些数据表明,miR-212通过靶向FOXA1抑制骨肉瘤细胞的活力和迁移。因此,miR-212可能成为骨肉瘤治疗的潜在候选物。