Open Access Highly Accessed Research article

MiR-200a inhibits epithelial-mesenchymal transition of pancreatic cancer stem cell

Yuhua Lu123, Jingjing Lu1, Xiaohong Li1, Hui Zhu1, Xiangjun Fan2, Shajun Zhu2, Yao Wang2, Qingsong Guo2, Lei Wang2, Yan Huang2, Mingyan Zhu2* and Zhiwei Wang2*

Author Affiliations

1 Surgical comprehensive laboratory, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province 226001, P. R. China

2 Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province 226001, P. R. China

3 Visitor scholar of Wake Forest Institute for Regenerative Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA

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BMC Cancer 2014, 14:85  doi:10.1186/1471-2407-14-85

Published: 12 February 2014



Pancreatic cancer is one of the most aggressive cancers, and the aggressiveness of pancreatic cancer is in part due to its intrinsic and extrinsic drug resistance characteristics, which are also associated with the acquisition of epithelial-to-mesenchymal transition (EMT). Increasing evidence suggests that EMT-type cells share many biological characteristics with cancer stem-like cells. And miR-200 has been identified as a powerful regulator of EMT.


Cancer Stem Cells (CSCs) of human pancreatic cancer cell line PANC-1 were processed for CD24, CD44 and ESA multi-colorstaining, and sorted out on a BD FACS Aria II machine. RT-qPCR was performed using the miScript PCR Kit to assay the expression of miR-200 family. In order to find the role of miR-200a in the process of EMT, miR-200a mimic was transfected to CSCs.


Pancreatic cancer cells with EMT phenotype displayed stem-like cell features characterized by the expression of cell surface markers CD24, CD44 and epithelial-specific antigen (ESA), which was associated with decreased expression of miR-200a. Moreover, overexpression of miR-200a was resulted in down-regulation of N-cadherin, ZEB1 and vimentin, but up-regulation of E-cadherin. In addition, miR-200a overexpression inhibited cell migration and invasion in CSCs.


In our study, we found that miR-200a played an important role in linking the characteristics of cancer stem-like cells with EMT-like cell signatures in pancreatic cancer. Selective elimination of cancer stem-like cells by reversing the EMT phenotype to mesenchymal-to-epithelial transition (MET) phenotype using novel agents would be useful for prevention and/or treatment of pancreatic cancer.

CSC; EMT; Pancreatic cancer; miR-200a