Format

Send to

Choose Destination
Int J Clin Exp Pathol. 2015 Sep 1;8(9):11224-9. eCollection 2015.

MiR-223 inhibited cell metastasis of human cervical cancer by modulating epithelial-mesenchymal transition.

Author information

1
Department of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University Guangzhou 510282, People's Republic of China ; Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University Xiamen 361003, People's Republic of China.
2
Department of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University Guangzhou 510282, People's Republic of China.
3
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University Xiamen 361003, People's Republic of China.
4
Central Laboratory, The First Affiliated Hospital of Xiamen University Xiamen 361003, People's Republic of China.
5
Department of Pathology, The First Affiliated Hospital of Xiamen University Xiamen 361003, People's Republic of China.

Abstract

Accumulating evidence have emerged important roles for microRNAs (miRNAs) participating in epithelial-mesenchymal transition (EMT) process and are associated with metastasis in cervical cancer. We hypothesized that miR-223 played an important role in cell metastasis of cervical cancer. Here, we found miR-223 was downregulated in human cervical cancer cell lines and clinical tumor tissues. Result of wound healing and cell migration assays revealed that miR-223 inhibited cell migration, whereas miR-223-in showed the opposite effect. In terms of mechanism, miR-223 influenced the expression of the EMT-associated proteins by upregulating the epithelial markers E-cadherin and α-cadherin and downregulating the mesenchymal marker vimentin. In conclusion, miR-223 inhibited cell metastasis of human cervical cancer by modulating epithelial-mesenchymal transition.

KEYWORDS:

cell metastasis; human cervical cancer; miR-223

PMID:
26617846
PMCID:
PMC4637661
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center