LncRNA ABCA9-AS1 as a ceRNA Promotes Gastric Cancer Progression by Sponging miR-497-5p to Regulate KIF23 Expression.

IF 2.5 4区医学 Q3 ONCOLOGY

Current cancer drug targets Pub Date : 2026-07-22 DOI:10.2174/0115680096455467260703054748

Yiwen Wu, Yiniu Xia, Hanyu Liu, Shilin Wen, Keming Zhong, Qianwen Xiao, Zhou Wang, Xiaoyan Yang, Zhizhong Xie

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引用次数: 0

Abstract

Introduction: Long noncoding RNAs (lncRNAs) have emerged as important modulators in the molecular pathology of cancer. lncRNA ABCA9-AS1 is a newly identified lncRNA, and its role in gastric cancer has not yet been reported.

Objective: To investigate the effects of lncRNA ABCA9-AS1 on the proliferation and metastasis of gastric cancer cells and to explore its role in the miR-497-5p/KIF23 signalling cascade.

Methods: A gastric cancer-specific ceRNA network (lncRNA-miRNA-mRNA) was constructed using RNA-seq and miRNA-seq data from TCGA. qRT-PCR was used to detect the expression levels of the target genes in gastric cancer cells (AGS, HGC-27, MKN28) and human gastric mucosal epithelial cells (GES-1). Knockdown of lncRNA ABCA9-AS1 was achieved using specific siRNA, while overexpression of KIF23 was achieved using a pcDNA3.1-based overexpression plasmid. The proliferative capacity of gastric cancer cells was assessed using CCK-8 and colony formation assays. Cell migration and invasion were evaluated by Transwell migration and Matrigel invasion assays, respectively.

Results: A gastric cancer-specific lncRNA-associated ceRNA network was constructed. qRT-PCR showed significant upregulation of lncRNA ABCA9-AS1 in gastric cancer cells (AGS, HGC-27, MKN28), with concomitant downregulation of miR-497-5p and upregulation of KIF23. In AGS cells, ABCA9-AS1 knockdown increased miR-497-5p expression and reduced KIF23 expression, while miR-497-5p mimics suppressed KIF23 expression. Functional assays confirmed that ABCA9-AS1 knockdown and miR-497-5p overexpression inhibited the proliferation, migration, and invasion of AGS cells. Conversely, KIF23 restoration or miR-497-5p inhibition reversed these effects, as did KIF23 co-expression with miR-497-5p mimics.

Discussion: Our results highlight lncRNA ABCA9-AS1 as a novel and promising prognostic biomarker that promotes gastric cancer progression by acting as a ceRNA to modulate the miR-497-5p/KIF23 axis.

Conclusion: lncRNA ABCA9-AS1 is aberrantly upregulated in gastric cancer. As a ceRNA, it sponges miR-497-5p to increase KIF23 expression and enhance the proliferation, migration, and invasion of gastric cancer cells.

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LncRNA ABCA9-AS1作为ceRNA通过海绵miR-497-5p调节KIF23表达促进胃癌进展

长链非编码rna （Long noncoding rna, lncRNAs）已成为癌症分子病理中重要的调节因子。lncRNA ABCA9-AS1是新发现的lncRNA，其在胃癌中的作用尚未见报道。目的：研究lncRNA ABCA9-AS1对胃癌细胞增殖转移的影响，并探讨其在miR-497-5p/KIF23信号级联中的作用。方法：利用TCGA的RNA-seq和miRNA-seq数据构建胃癌特异性ceRNA网络（lncRNA-miRNA-mRNA）。采用qRT-PCR检测靶基因在胃癌细胞（AGS、HGC-27、MKN28）和人胃粘膜上皮细胞（GES-1）中的表达水平。使用特异性siRNA实现lncRNA ABCA9-AS1的敲低，而使用基于pcdna3.1的过表达质粒实现KIF23的过表达。采用CCK-8和集落形成试验评估胃癌细胞的增殖能力。采用Transwell迁移法和Matrigel侵袭法分别评价细胞迁移和侵袭。结果：构建了胃癌特异性lncrna相关的ceRNA网络。qRT-PCR结果显示，lncRNA ABCA9-AS1在胃癌细胞（AGS、HGC-27、MKN28）中显著上调，同时miR-497-5p下调，KIF23上调。在AGS细胞中，ABCA9-AS1敲低miR-497-5p表达增加，KIF23表达降低，而miR-497-5p模拟物抑制KIF23表达。功能分析证实ABCA9-AS1敲低和miR-497-5p过表达抑制AGS细胞的增殖、迁移和侵袭。相反，KIF23恢复或miR-497-5p抑制逆转了这些作用，KIF23与miR-497-5p模拟物的共表达也逆转了这些作用。讨论：我们的研究结果突出了lncRNA ABCA9-AS1作为一种新的和有前途的预后生物标志物，通过作为ceRNA调节miR-497-5p/KIF23轴来促进胃癌进展。结论：lncRNA ABCA9-AS1在胃癌中表达异常上调。作为一种ceRNA，它通过吞噬miR-497-5p来提高KIF23的表达，增强胃癌细胞的增殖、迁移和侵袭能力。

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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来源期刊

Current cancer drug targets 医学-肿瘤学

CiteScore

5.40

自引率

0.00%

发文量

105

审稿时长

1 months

期刊介绍： Current Cancer Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular drug targets involved in cancer, e.g. disease specific proteins, receptors, enzymes and genes. Current Cancer Drug Targets publishes original research articles, letters, reviews / mini-reviews, drug clinical trial studies and guest edited thematic issues written by leaders in the field covering a range of current topics on drug targets involved in cancer. As the discovery, identification, characterization and validation of novel human drug targets for anti-cancer drug discovery continues to grow; this journal has become essential reading for all pharmaceutical scientists involved in drug discovery and development.