TY - JOUR
T1 - Thrombomodulin mediates the migration of cervical cancer cells through the regulation of epithelial-mesenchymal transition biomarkers
AU - Tai, Cheng-Jeng
AU - Cheng, Chao-Wen
AU - Su, Hou Yu
AU - Chen, Wei-Yu
AU - Wu, Chun Te
AU - Lin, Feng-Yen
AU - Wang, Chien Kai
AU - Tai, Chen-Jei
AU - Wei, Po-Li
PY - 2014/1
Y1 - 2014/1
N2 - Thrombomodulin (TM) has been shown to regulate many physiological and pathological processes, including inflammation, thrombosis, and tumor progression. TM is also a natural anticoagulant that maintains circulatory homeostasis in endothelial cells. However, little is known regarding the role of TM in the progression and metastasis of cervical cancer. TM-specific RNA interference and a cDNA expression vector were used to manipulate TM expression in cervical cancer cells. Cell growth and cell migration were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, transwell migration assays, and a biosensor system. TM silencing did not affect the growth rate of the cells. However, cell migration was dramatically enhanced after silencing of TM in HeLa cells. The overexpression of TM in cervical cancer cells only slightly influenced their proliferative capacity. After overexpression of TM in HeLa cells, their migratory capability was suppressed. Furthermore, we found that the decreased expression of E-cadherin and increase of zeb-1 and snail expression in TM-silenced cells which may be correlated with the results of knocking-down TM increases the migratory ability in this study. Our results demonstrate that TM may slightly regulate the growth but played the important role in the migratory ability of cervical cancer cells, suggesting that TM could potentially serve as a novel prognostic and therapeutic target in cervical cancer.
AB - Thrombomodulin (TM) has been shown to regulate many physiological and pathological processes, including inflammation, thrombosis, and tumor progression. TM is also a natural anticoagulant that maintains circulatory homeostasis in endothelial cells. However, little is known regarding the role of TM in the progression and metastasis of cervical cancer. TM-specific RNA interference and a cDNA expression vector were used to manipulate TM expression in cervical cancer cells. Cell growth and cell migration were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, transwell migration assays, and a biosensor system. TM silencing did not affect the growth rate of the cells. However, cell migration was dramatically enhanced after silencing of TM in HeLa cells. The overexpression of TM in cervical cancer cells only slightly influenced their proliferative capacity. After overexpression of TM in HeLa cells, their migratory capability was suppressed. Furthermore, we found that the decreased expression of E-cadherin and increase of zeb-1 and snail expression in TM-silenced cells which may be correlated with the results of knocking-down TM increases the migratory ability in this study. Our results demonstrate that TM may slightly regulate the growth but played the important role in the migratory ability of cervical cancer cells, suggesting that TM could potentially serve as a novel prognostic and therapeutic target in cervical cancer.
KW - Cervical cancer
KW - EMT
KW - Migration
KW - Thrombomodulin
UR - http://www.scopus.com/inward/record.url?scp=84893732359&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84893732359&partnerID=8YFLogxK
U2 - 10.1007/s13277-013-1005-7
DO - 10.1007/s13277-013-1005-7
M3 - Article
C2 - 23881386
AN - SCOPUS:84893732359
VL - 35
SP - 47
EP - 54
JO - Oncodevelopmental Biology and Medicine
JF - Oncodevelopmental Biology and Medicine
SN - 1010-4283
IS - 1
ER -