BACKGROUND Previous studies have shown that long noncoding RNA (lncRNA) LINC00483 was aberrantly expressed in human cancers, including gastric cancer. However, the regulatory mechanism of this lncRNA in gastric cancer remains largely unknown. The present study aimed to investigate the effect of LINC00483 on gastric cancer development and explore the potential regulatory network of LINC00483/microRNA (miR)-490-3p/mitogen-activated protein kinase 1 (MAPK1). METHODS Thirty patients with gastric cancer were recruited for tissues collection. The expression levels of LINC00483, miR-490-3p and MAPK1 were detected by quantitative real-time polymerase chain reaction or western blot. Cell viability, apoptosis, migration and invasion were determined by MTT, flow cytometry, transwell assays and western blot, respectively. The target association between miR-490-3p and LINC00483 or MAPK1 was confirmed by luciferase reporter assay. Xenograft model was established to assess the function of LINC00483 in vivo. RESULTS LINC00483 and MAPK1 levels were increased in gastric cancer tissues and cells. Knockdown of LINC00483 or MAPK1 inhibited cells viability, migration and invasion but promoted apoptosis in gastric cancer cells. Moreover, MAPK1 overexpression attenuated the effect of LINC00483 knockdown on gastric cancer development. LINC00483 could increase MAPK1 expression by competitively sponging miR-490-3p. miR-490-3p overexpression suppressed gastric cancer development, which was abated by introduction of LINC00483. Besides, inhibition of LINC00483 decreased xenograft tumor growth by regulating miR-490-3p/MAPK1 axis. CONCLUSION Knockdown of LINC00483 inhibited gastric cancer development in vitro and in vivo by increasing miR-490-3p and decreasing MAPK1, elucidating a novel mechanism for understanding the development of gastric cancer.

中文翻译：

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LncRNA LINC00483通过使miR-490-3p海绵化来调节MAPK1表达，从而促进胃癌的发展。

背景技术以前的研究表明，长的非编码RNA（lncRNA）LINC00483在包括胃癌在内的人类癌症中异常表达。但是，这种lncRNA在胃癌中的调控机制仍然未知。本研究旨在调查LINC00483对胃癌发展的影响，并探索LINC00483 / microRNA（miR）-490-3p /促分裂原活化蛋白激酶1（MAPK1）的潜在调控网络。方法收集30例胃癌患者的组织。通过定量实时聚合酶链反应或western blot检测LINC00483，miR-490-3p和MAPK1的表达水平。细胞活力，凋亡，迁移和侵袭分别通过MTT，流式细胞术，transwell测定和western blot测定。通过荧光素酶报告基因分析证实了miR-490-3p与LINC00483或MAPK1之间的靶标关联。建立异种移植模型以评估LINC00483在体内的功能。结果胃癌组织和细胞中LINC00483和MAPK1水平升高。敲低LINC00483或MAPK1抑制细胞活力，迁移和侵袭，但促进胃癌细胞凋亡。此外，MAPK1过表达减弱了LINC00483敲低对胃癌发展的影响。LINC00483可通过竞争性增强miR-490-3p的表达来增加MAPK1的表达。miR-490-3p的过表达抑制了胃癌的发展，这通过引入LINC00483得以缓解。此外，通过调节miR-490-3p / MAPK1轴，抑制LINC00483可以降低异种移植瘤的生长。