Increasing evidence indicates that aberrantly expressed microRNAs play a role in tumorigenesis and progression of gastric cancer. Recently, a novel cancer-related microRNA, miR-621, was found to be involved in cancer pathogenesis. However, the precise molecular mechanisms underlying the oncogenic activity of miR-621 remain unclear and require further investigation. In the current study, we demonstrate that miR-621 expression is downregulated in gastric cancer tissues and cell lines, and its reduction is associated with malignant clinical features including tumor size, lymph node metastasis, tumor-node-metastasis stage and poor prognosis. Functional studies involving gain- and loss-of-function experiments revealed that miR-621 represses cell viability, colony formation, cell cycle progression and proliferation in vitro, and miR-621 overexpression inhibited tumor growth in a gastric cancer xenograft model. SYF2 was identified as a direct target gene of miR-621 in gastric cancer. MiR-621 directly interacts with the SYF2 3'-UTR and post-transcriptionally repressed SYF2 expression in gastric cancer cells. SYF2 was significantly overexpressed in gastric cancer tissues and negatively correlated with miR-621 expression. Moreover, inhibition of SYF2 expression reversed the effects of miR-621 loss in gastric cancer cells. SYF2 overexpression was similar to that induced by miR-621 loss in gastric cancer. Taken together, these studies suggest that miR-621 may be a viable therapeutic target in gastric cancer.

中文翻译：

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MicroRNA-621通过靶向SYF2抑制胃癌细胞的生长。

越来越多的证据表明，异常表达的microRNA在胃癌的发生和发展中起作用。最近，发现一种新型的与癌症相关的微小RNA miR-621与癌症的发病机制有关。然而，miR-621致癌活性的确切分子机制仍不清楚，需要进一步研究。在当前的研究中，我们证明了miR-621在胃癌组织和细胞系中的表达下调，其减少与恶性临床特征有关，包括肿瘤大小，淋巴结转移，肿瘤结点转移阶段和不良预后。涉及功能获得和丧失功能实验的功能研究表明，miR-621在体外可抑制细胞活力，集落形成，细胞周期进程和增殖，miR-621和过表达抑制胃癌异种移植模型中肿瘤的生长。SYF2被鉴定为miR-621在胃癌中的直接靶基因。MiR-621直接与SYF2 3'-UTR相互作用，并在转录后抑制胃癌细胞中SYF2的表达。SYF2在胃癌组织中显着过表达，并且与miR-621表达负相关。此外，SYF2表达的抑制逆转了miR-621丢失在胃癌细胞中的作用。SYF2过表达与miR-621缺失引起的胃癌相似。综上所述，这些研究表明miR-621可能是胃癌的可行治疗靶标。MiR-621直接与SYF2 3'-UTR相互作用，并在转录后抑制胃癌细胞中SYF2的表达。SYF2在胃癌组织中显着过表达，并且与miR-621表达负相关。此外，SYF2表达的抑制逆转了miR-621丢失在胃癌细胞中的作用。SYF2过表达与miR-621缺失引起的胃癌相似。综上所述，这些研究表明miR-621可能是胃癌的可行治疗靶标。MiR-621直接与SYF2 3'-UTR相互作用，并在转录后抑制胃癌细胞中SYF2的表达。SYF2在胃癌组织中显着过表达，并且与miR-621表达负相关。此外，SYF2表达的抑制逆转了miR-621丢失在胃癌细胞中的作用。SYF2过表达与miR-621缺失引起的胃癌相似。综上所述，这些研究表明miR-621可能是胃癌的可行治疗靶标。SYF2过表达与miR-621缺失引起的胃癌相似。综上所述，这些研究表明miR-621可能是胃癌的可行治疗靶标。SYF2过表达与miR-621缺失引起的胃癌相似。综上所述，这些研究表明miR-621可能是胃癌的可行治疗靶标。