详细信息
MicroRNA-330靶向EGR-2基因抑制胃癌细胞生长和迁移 被引量:6
MicroRNA-330 inhibits growth and migration of gastric cancer cells by directly targeting EGR-2
文献类型:期刊文献
中文题名:MicroRNA-330靶向EGR-2基因抑制胃癌细胞生长和迁移
英文题名:MicroRNA-330 inhibits growth and migration of gastric cancer cells by directly targeting EGR-2
作者:赵蓉蓉[1];付兆媛[2]
第一作者:赵蓉蓉
机构:[1]甘肃中医药大学附属医院检验科,甘肃兰州730000;[2]甘肃中医药大学附属医院肿瘤科,甘肃兰州730000
第一机构:甘肃中医药大学第二附属医院
年份:2019
卷号:35
期号:6
起止页码:1055
中文期刊名:中国病理生理杂志
外文期刊名:Chinese Journal of Pathophysiology
收录:CSTPCD;;北大核心:【北大核心2017】;CSCD:【CSCD2019_2020】;
基金:甘肃省自然科学基金资助项目(No.1208RJZA181;No.17JR5RA173)
语种:中文
中文关键词:微小RNA-330;胃癌;细胞活力;细胞迁移;EGR-2基因
外文关键词:MicroRNA-330;Gastric cancer;Cell viability;Cell migration;EGR-2 gene
摘要:目的:探讨微小RNA-330(microRNA-330,miR-330)在胃癌进展中的作用和意义。方法:收集甘肃中医药大学附属医院肿瘤科48例胃癌组织标本及配对癌旁组织,通过RT-qPCR检测miR-330的表达水平;RT-qPCR检测人类正常胃黏膜上皮细胞GES-1和胃癌细胞中miR-330的相对表达水平;在胃癌细胞中转染miR-330 inhibitor或miR-330 mimic后,采用CCK-8法、平板集落形成实验和Transwell实验检测细胞活力、集落形成能力和迁移能力的变化;进一步采用miRanda靶基因预测数据库预测miR-330的靶基因。结果:miR-330在胃癌组织和癌细胞中低表达(P<0.05),且表达水平与肿瘤大小、淋巴结转移、病理分级和T分期负相关(P<0.05)。转染miR-330 inhibitor后,胃癌细胞的活力、集落形成能力和迁移能力显著升高(P<0.05);转染miR-330 mimic后,胃癌细胞的活力、集落形成能力和迁移能力显著降低(P<0.05);miR-330的靶基因为EGR-2。结论:miR-330可抑制胃癌细胞的恶性表型,其分子机制可能与靶基因EGR2相关。miR-330或许可成为胃癌的一个诊断指标和治疗靶点。
AIM: To explore the function and significance of microRNA-330(miR-330) in the development of gastric cancer. METHODS: Forty-eight cases of gastric cancer tissues and paired adjacent tissues were collected in Department of Oncology, Affiliated Hospital of Gansu University of Chinese Medicine, and the expression levels of miR-330 were detected by RT-qPCR. The expression levels of miR-330 in the gastric cancer cells and human gastric epithelial GES-1 cells were evaluated by RT-qPCR. The viability, colony formation and migration of gastric cancer cells after transfected with miR-330 inhibitor or miR-330 mimic were analyzed by CCK-8 assay, colony formation assay and Transwell assay, respectively. Furthermore, miR-330 target gene was predicted by miRanda target gene prediction database. RESULTS: miR-330 expression was down-regulated both in gastric cancer tissues and gastric cancer cells(P<0.05). The expression levels of miR-330 were negatively associated with the tumor size, lymph metastasis, pathological grade stage and T stage(P<0.05). The viability, colony formation and migration of gastric cancer cells were significantly increased after transfected with miR-330 inhibitor(P<0.05). However, the viability, colony formation and migration of gastric cancer cells were significantly decreased after transfected with miR-330 mimic(P<0.05). Furthermore, EGR-2 was the direct target gene of miR-330. CONCLUSION: miR-330 suppresses gastric cancer cell growth and migration, and the mechanism may be related to its direct target gene EGR-2, suggesting that miR-330 may be used as a potential new target for diagnosis and targeted therapy for gastric cancer.
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