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- Title
miR-106b promotes cell invasion and metastasis via PTEN mediated EMT in ESCC.
- Authors
Zhang, Jianxiang; Chen, Danjie; Liang, Shuying; Wang, Jun; Liu, Can; Nie, Caiping; Shan, Zhengzheng; Wang, Liuxing; Fan, Qinxia; Wang, Feng
- Abstract
MicroRNA (miR)-106b serves an essential function in a variety of human cancer types, particularly in the process of invasion and metastasis. However, the function and mechanism of miR-106b in the invasion and metastasis of esophageal squamous cell carcinoma (ESCC) has remained elusive. In the present study, it was demonstrated that miR-106b was upregulated in ESCC tissues and cell lines. Furthermore, miR-106b expression in ESCC tissues was positively associated with lymphatic metastasis. Inhibition of miR-106b in EC-1 and EC9706 cells decreased not only the invasion and metastasis ability but also the proliferation ability of EC-1 and EC9706 cells. In addition, miR-106b had the ability to induce epithelial-to-mesenchymal transition (EMT) in EC-1 and EC9706 cells. In terms of the underlying mechanism, it was revealed that miR-106b promoted the invasion, metastasis and proliferation ability of EC-1 and EC9706 cells by directly targeting phosphatase and tension homolog (PTEN). Furthermore, miR-106b induced EMT in EC-1 and EC9706 cells by suppressing the expression of PTEN. In summary, the present study revealed that miR-106b contributed to invasion and metastasis in ESCC by regulating PTEN mediated EMT. Downregulation of miR-106b may be a novel strategy for preventing tumor invasion and metastasis.
- Subjects
MICRORNA; ESOPHAGEAL cancer; GENE expression; METASTASIS; CANCER invasiveness; PREVENTION
- Publication
Oncology Letters, 2018, Vol 15, Issue 4, p4619
- ISSN
1792-1074
- Publication type
Article
- DOI
10.3892/ol.2018.7861