Several long intergenic noncoding RNAs (lincRNAs) have been linked to carcinogenesis; however, little is known about the role of LINC00619 in gastric cancer (GC). LINC00619 was identified among differentially expressed lncRNAs linked to gastric cancer based on microarray analysis and its relationships with miR-224-5p and opioid binding protein/cell adhesion molecule-like gene (OPCML) were investigated. LINC00619, miR-224-5p, and OPCML expression were measured in GC tissues and cells. Ectopic expression and depletion experiments were conducted to assess the effects of LINC00619, miR-224-5p and OPCML on cell proliferation, invasion, migration and apoptosis as well as their effects on the expression of apoptosis- and metastasis-related genes (Bcl-2, Bax, MMP-2 and MMP-9). Tumorigenicity in the nude mice was also examined. Gastric cancer was characterized by downregulation of LINC00619 and OPCML and upregulation of miR-224-5p. Additionally, we found that miR-224-5p could interact with both LINC00619 and OPCML. Upregulation of LINC00619, which binds to miR-224-5p, led to decreased miR-224-5p expression while increasing the expression of OPCML, a target gene of miR-224-5p. Overexpression of LINC00619 or OPCML or downregulation of miR-224-5p suppressed cell proliferation, invasion, migration and tumorigenicity while promoting apoptosis in GC. Our results indicated that LINC00619 functions as a tumor suppressor in GC by impairing miR-224-5p-mediated inhibition of OPCML.

几种长的基因间非编码RNA（lincRNA）与致癌作用有关。然而，关于LINC00619在胃癌（GC）中的作用知之甚少。基于微阵列分析，在与胃癌相关的差异表达的lncRNAs中鉴定了LINC00619，并研究了其与miR-224-5p和阿片样物质结合蛋白/细胞粘附分子样基因（OPCML）的关系。在GC组织和细胞中测量了LINC00619，miR-224-5p和OPCML的表达。进行异位表达和耗竭实验以评估LINC00619，miR-224-5p和OPCML对细胞增殖，侵袭，迁移和凋亡的影响，以及它们对与凋亡和转移相关基因（Bcl-2 ，Bax，MMP-2和MMP-9）。还检查了裸鼠的致瘤性。胃癌的特征在于LINC00619和OPCML的下调和miR-224-5p的上调。此外，我们发现miR-224-5p可以与LINC00619和OPCML相互作用。与miR-224-5p结合的LINC00619的上调导致miR-224-5p表达降低，同时增加了miR-224-5p的靶基因OPCML的表达。LINC00619或OPCML的过表达或miR-224-5p的下调抑制细胞增殖，侵袭，迁移和致瘤性，同时促进GC中的细胞凋亡。我们的结果表明，LINC00619通过削弱miR-224-5p介导的OPCML抑制作用而在GC中起肿瘤抑制作用。它与miR-224-5p结合，导致miR-224-5p表达降低，同时增加了miR-224-5p的靶基因OPCML的表达。LINC00619或OPCML的过表达或miR-224-5p的下调抑制细胞增殖，侵袭，迁移和致瘤性，同时促进GC中的细胞凋亡。我们的结果表明，LINC00619通过削弱miR-224-5p介导的OPCML抑制作用而在GC中起肿瘤抑制作用。它与miR-224-5p结合，导致miR-224-5p表达降低，同时增加了miR-224-5p的靶基因OPCML的表达。LINC00619或OPCML的过表达或miR-224-5p的下调抑制细胞增殖，侵袭，迁移和致瘤性，同时促进GC中的细胞凋亡。我们的结果表明，LINC00619通过削弱miR-224-5p介导的OPCML抑制作用而在GC中起肿瘤抑制作用。