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首页> 外文期刊>Journal of cellular physiology. >miR-665 promotes the progression of gastric adenocarcinoma via elevating FAK activation through targeting SOCS3 and is negatively regulated by IncRNA MEG3
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miR-665 promotes the progression of gastric adenocarcinoma via elevating FAK activation through targeting SOCS3 and is negatively regulated by IncRNA MEG3

机译：mir - 665促进胃的进展通过提升FAK激活腺癌通过针对SOCS3和消极受IncRNA MEG3

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Studies have found that miR-665 acted as a tumor suppressor or an oncogene in different malignancies. miR-665 expression was elevated in gastric adenocarcinoma tissues; however, its role and mechanism in this disease are not fully clarified. The expression of miR-665 and its target gene was detected in human gastric adenocarcinoma tissues and cells. Moreover, we analyzed the effects of miR-665 on the proliferation, migration, and epithelial-mesenchymal transition (EMT) of gastric adenocarcinoma cells as well as tumor growth in vivo. The mechanisms of miR-665 in gastric adenocarcinoma were investigated by using molecular biology techniques. We found miR-665 was upregulated and suppressor of cytokine signaling 3 (SOCS3) was downregulated in gastric adenocarcinoma tissues and cells. Elevated miR-665 was positively correlated with tumor size, lymph node metastasis, invasion depth, TNM stage, and poor differentiation in gastric adenocarcinoma patients. Overexpression of miR-665 promoted, whereas knockdown of miR-665 suppressed the proliferation, migration, and EMT of gastric adenocarcinoma cells. Furthermore, we demonstrated that miR-665 functioned through targeting SOCS3, followed by activation of the FAK/ Src signaling pathway in gastric adenocarcinoma cells. miR-665 antagomir inhibited tumor growth as well as the activation of the FAK/Src pathway but increased SOCS3 expression in nude mice. In addition, miR-665 expression was negatively regulated by long noncoding RNA maternally expressed gene 3 (MEG3). In conclusion, miR-665 acted as an oncogene in gastric adenocarcinoma by inhibiting SOCS3 followed by activation of the FAK/Src pathway and it was negatively modulated by MEG3. miR-665 may be a promising therapeutic target for the treatment of gastric adenocarcinoma.
机译：研究发现,mir - 665作为一个肿瘤抑制或致癌基因在不同恶性肿瘤。胃腺癌组织;在这种疾病还没有完全和机制澄清。目标基因被发现在人类胃腺癌组织和细胞。分析了mir - 665对增殖、迁移和epithelial-mesenchymal过渡(EMT)胃腺癌的细胞以及肿瘤增长的体内。胃腺癌被使用了分子生物学技术。是调节和抑制细胞因子信号3 (SOCS3)在胃表达下调腺癌组织和细胞。mir - 665呈正相关,肿瘤大小、淋巴结转移、TNM侵入深度阶段,可怜的胃中分化腺癌患者。mir - 665提升,而击倒mir - 665抑制增殖、迁移和EMT胃腺癌的细胞。表明,mir - 665功能通过针对SOCS3,紧随其后的是激活的FAK在胃/ Src信号通路腺癌的细胞。肿瘤生长以及激活FAK / Src途径但SOCS3表达增加裸小鼠。消极受长非编码RNA母亲般地表达基因3 (MEG3)。结论,mir - 665作为一个致癌基因通过抑制SOCS3胃腺癌其次是FAK / Src通路和激活它被MEG3负面调制。是一个有前途的治疗目标胃腺癌的治疗。

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