@Article{096504017X15009778205068,
AUTHOR = {Waraporn Saentaweesuk, Norie Araki, Kulthida Vaeteewoottacharn, Atit Silsirivanit, Wunchana Seubwai, Chutima Talabnin, Kanha Muisuk, Banchob Sripa, Sopit Wongkham, Seiji Okada, Chaisiri Wongkham},
TITLE = {Activation of Vimentin Is Critical to Promote a Metastatic Potential  of Cholangiocarcinoma Cells},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {4},
PAGES = {605--616},
URL = {http://www.techscience.com/or/v26n4/56673},
ISSN = {1555-3906},
ABSTRACT = {Cholangiocarcinoma (CCA) is a highly metastatic tumor, and the majority of patients with CCA have a short 
survival time because there are no available effective treatments. Hence, a better understanding regarding CCA 
metastasis may provide an opportunity to improve the strategies for treatment. A comparison study between the 
highly metastatic cells and their parental cells is an approach to uncover the molecular mechanisms underlying 
the metastatic process. In the present study, a lung metastatic CCA cell line, KKU-214L5, was established by 
the in vivo selection of the tail vein-injected mouse model. KKU-214L5 cells possessed mesenchymal 
spindle-like morphology with higher migration and invasion abilities in vitro than the parental cells (KKU-214). 
KKU-214L5 also exhibited extremely aggressive lung colonization in the tail vein-injected metastatic model. 
Epithelial–mesenchymal transition (EMT) was clearly observed in KKU-214L5 cells. Significant downregulation of epithelial markers (ZO-1 and claudin-1), with unique upregulation of E-cadherin and mesenchymal 
markers (vimentin, b-catenin, and slug), was observed in KKU-214L5. Increasing MMP-2 and MMP-9 activities and CD147 expression reflected the high invasion activity in KKU-214L5 cells. Suppression of vimentin 
using siRNA significantly decreased the migration and invasion capabilities of KKU-214L5 to almost the basal 
levels of the parental cells without any change on the expression levels of other EMT markers and the activities of MMPs. These results suggest that vimentin activation is essential to potentiate the metastatic characters 
of CCA cells, and suppression of vimentin expression could be a potential strategy to improve the treatment of 
CCA, a highly metastatic cancer.},
DOI = {10.3727/096504017X15009778205068}
}