LncRNA RGMB-AS1 up-regulates ANKRD1 Through Competitively Sponging miR-3614-5p to Promote OSA Cell Proliferation and Invasion

被引:8
|
作者
Yin, Peng [1 ]
Tong, Changgui [2 ]
机构
[1] Dalian Med Univ, Hosp 2, Dept Orthopaed, Dalian, Liaoning, Peoples R China
[2] Dalian Med Univ, Hosp 2, Dept Hand & Foot Microsurg, 467 Zhongshan Rd, Dalian 116023, Liaoning, Peoples R China
关键词
lncRNA RGMB-AS1; FOXA1; miR-3614-5p; ANKRD1; OSA; CANCER; CERNA;
D O I
10.1016/j.arcmed.2021.08.004
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background. Osteosarcoma (OSA) is associated with unfavorable prognosis. The over-all survival rate for patients with OSA recurrence or metastasis is only about 20%. Long non-coding RNAs (lncRNAs) significantly function in gene expression and the progression of various cancers including OSA.Methods. The expression of repulsive guidance molecule BMP co-receptor b antisense RNA 1 (RGMB-AS1) was detected in OSA cells via qRT-PCR. Western blot assay exposed the protein level of ankyrin repeat domain 1 (ANKRD1). The function assays showed the role of RGMB-AS1, miR-3614-5p, ANKRD1 on OSA cell proliferation and invasion. Subcellular Fraction assay was conducted to detect RGMB-AS1 localization. Rescue assays manifested the mechanism of RGMB-AS1/miR-3614-5p/ANKRD1 axis in OSA cells. Results. FOXA1-activated RGMB-AS1 positively regulated OSA cell progression includ-ing proliferation and invasion but negatively modulated apoptosis. miR-3614-5p inter-acted with RGMB-AS1 and functioned as the tumor suppressor in OSA cells. ANKRD1 was targeted by miR-3614-5p and was negatively interacted by miR-3614-5p. RGMB-AS1 and ANKRD1 competitively bound with miR-3614-5p. The suppression of silenc-ing RGMB-AS1 on OSA cell progression was rescued by ANKRD1 overexpression or miR-3614-5p down-regulation.Conclusions. FOXA1-activated RGMB-AS1 promoted cell proliferation and invasion in OSA via miR-3614-5p/ANKRD1 pathway.(c) 2021 Instituto Mexicano del Seguro Social (IMSS). Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:131 / 137
页数:7
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