LncRNA AFAP1-AS1 Knockdown Represses Cell Proliferation, Migration, and Induced Apoptosis in Breast Cancer by Downregulating SEPT2 Via Sponging miR-497-5p.

Cancer biotherapy & radiopharmaceuticals Pub Date : 2022-10-01 Epub Date: 2020-09-21 DOI:10.1089/cbr.2020.3688
Bo Cai, Xichao Wang, Qing'ao Bu, Peng Li, Qingze Xue, Jun Zhang, Pengpeng Ding, Diwen Sun
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引用次数: 11

Abstract

Background: Long non-coding RNA actin filament-associated protein1-antisense RNA 1 (AFAP1-AS1) was confirmed to be associated with tumorigenesis. However, the role of AFAP1-AS1 in breast cancer was little known. Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the levels of AFAP1-AS1, microRNA-497-5p (miR-497-5p), and Septin 2 (SEPT2) in breast cancer tissues and cells. The cell proliferation, migration, and apoptosis were tested by Methylthiazolyldiphenyl-tetrazolium bromide (MTT), Transwell and Flow cytometry assays, respectively. The targeting relationship between genes was predicted by StarBase v.3.0 and confirmed by dual-luciferase reporter assay. Pearson's correlation coefficient was applied to examine the correlation between the two groups. SEPT2 protein expression was evaluated by Western blot. Xenograft models were established to investigate the role of AFAP1-AS1 knockdown in vivo. Results: AFAP1-AS1 was upregulated in breast cancer tissues and cells, and AFAP1-AS1 knockdown could hinder proliferation and migration of breast cancer cells, and contribute to cell apoptosis. MiR-497-5p, which was downregulated in breast cancer, was verified to be a target of AFAP1-AS1 and inversely correlated with AFAP1-AS1 expression. SEPT2, as a target gene of miR-497-5p, was negatively regulated by miR-497-5p and positively correlated with AFAP1-AS1 expression. Importantly, AFAP1-AS1 could upregulate SEPT2 expression by sponging miR-497-5p, and modulate cell progression by regulation of the miR-497-5p/SEPT2 axis in breast cancer. Conclusion: AFAP1-AS1 knockdown repressed the progression of breast cancer cells by sponging miR-497-5p and downregulating SEPT2.

LncRNA AFAP1-AS1敲低通过海绵miR-497-5p下调SEPT2抑制乳腺癌细胞增殖、迁移和诱导凋亡
背景:长链非编码RNA肌动蛋白丝相关蛋白-反义RNA 1 (AFAP1-AS1)被证实与肿瘤发生有关。然而,AFAP1-AS1在乳腺癌中的作用知之甚少。材料与方法:采用实时定量聚合酶链反应(qRT-PCR)检测乳腺癌组织和细胞中AFAP1-AS1、microRNA-497-5p (miR-497-5p)、Septin 2 (SEPT2)水平。分别采用甲基噻唑基二苯四唑溴化铵(MTT)、Transwell和流式细胞术检测细胞增殖、迁移和凋亡。通过StarBase v.3.0预测基因间的靶向关系,并通过双荧光素酶报告基因试验证实。采用Pearson相关系数检验两组间的相关性。Western blot检测SEPT2蛋白表达。建立异种移植模型,研究AFAP1-AS1敲低在体内的作用。结果:AFAP1-AS1在乳腺癌组织和细胞中表达上调,敲低AFAP1-AS1可抑制乳腺癌细胞的增殖和迁移,促进细胞凋亡。在乳腺癌中下调的MiR-497-5p被证实是AFAP1-AS1的靶标,并且与AFAP1-AS1的表达呈负相关。SEPT2作为miR-497-5p的靶基因,受到miR-497-5p的负调控,与AFAP1-AS1表达呈正相关。重要的是,AFAP1-AS1可以通过海绵化miR-497-5p上调SEPT2的表达,并通过调节乳腺癌中miR-497-5p/SEPT2轴调节细胞进展。结论:AFAP1-AS1敲低通过海绵化miR-497-5p和下调SEPT2抑制乳腺癌细胞的进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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