MicroRNA-205 suppresses the invasion and epithelial-mesenchymal transition of human gastric cancer cells

被引:33
作者
Xu, Chang [1 ]
Li, Ming'e [2 ]
Zhang, Lin [1 ]
Bi, Yueyang [3 ]
Wang, Peiyuan [1 ]
Li, Jun [1 ]
Jiang, Xingyue [1 ]
机构
[1] Binzhou Med Univ, Affiliated Hosp, Dept Radiol, 661 Huangheer Rd, Binzhou 256603, Shandong, Peoples R China
[2] Binzhou Med Univ, Affiliated Hosp, Dept Gerontol, Binzhou 256603, Shandong, Peoples R China
[3] Binzhou Med Univ, Affiliated Hosp, Dept Resp Med, Binzhou 256603, Shandong, Peoples R China
关键词
gastric cancer; microRNA-205; epithelial-mesenchymal transition; metastasis; PROSTATE-CANCER; DOWN-REGULATION; METASTASIS; MIR-205; ZEB1; PROLIFERATION; PROGRESSION; EXPRESSION; MARKERS; PROTEIN;
D O I
10.3892/mmr.2016.5118
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Distant metastasis is the predominant pattern of gastric cancer (GC) recurrence, and is the most common cause of cancer-associated mortality. Accumulating evidence has suggested that aberrant activation of epithelial-mesenchymal transition has a crucial role in the genesis, invasion and metastasis of various types of cancer, including GC. Using Cell Counting kit-8 and Transwell assays, the effects of microRNA (miR)-205 on the proliferation, migration and invasion of NCI-H87 GC cells were determined, and the potential underlying mechanisms were explored. The results of the present study demonstrated that miR-205, which has been reported to function as a tumor suppressor in various types of cancer, significantly suppressed the migration and invasion of GC cells, which may be correlated with its suppressive effects on EMT. Upon transfection with miR-205, the epithelial marker CDH1 (E-cadherin) was upregulated, and the mesenchymal markers CDH2 (N-cadherin) and vimentin were suppressed. Furthermore, zinc-finger E-box-binding homeobox factor-1 (ZEB1) was identified as a putative target gene of miR-205 in GC, which may be associated with its suppressive effects. The results of the present study may provide novel diagnostic and therapeutic options for the treatment of human GC.
引用
收藏
页码:4767 / 4773
页数:7
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