Thrombomodulin mediates the progression of epithelial ovarian cancer cells.

Abstract

Thrombomodulin (TM), a natural anticoagulation factor, maintains circulation homeostasis in endothelial cells. TM has additional roles in modulating inflammation, thrombosis, and carcinogenesis. However, there is little information on the role of TM in the progression and metastasis of ovarian cancer. RNA silencing and cDNA expression vectors were used to manipulate target gene expression in ovarian cancer cells. Cell growth and migration were evaluated by an MTT assay, a wound-healing migration assay, a transwell migration assay, and a biosensor system. In this study, we found that TM silencing may enhance the growth rate of cells. The migratory ability of ovarian cancer cells was enhanced dramatically after TM silencing. TM overexpression in ovarian cells suppressed the proliferation and migration capability. Furthermore, we found that skov-3 cells treated with TM shRNA expressed high levels of fibronectin and vimentin and that the expression of these markers correlated positively with their migratory ability. Our results demonstrate that TM expression may regulate cell growth and migration in ovarian cancer cells. This finding suggests that TM may be a novel prognostic and therapeutic target for ovarian cancer.

• Authors: Lu-Min Chen, Weu Wang, Jen-Chih Lee, Feng-Hsiang Chiu, Chun-Te Wu, Cheng-Jeng Tai, Chien-Kai Wang, Chen-Jei Tai, Ming-Te Huang, Yu-Jia Chang
• Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine (Tumour Biol) Vol. 34 Issue 6 Pg. 3743-51 (Dec 2013) ISSN: 1423-0380 [Electronic] Netherlands
• PMID: 23918310 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Biomarkers, Tumor
• Fibronectins
• Thrombomodulin
• Vimentin

Topics

• Biomarkers, Tumor (genetics, metabolism)
• Blotting, Western
• Cell Line, Tumor
• Cell Movement (genetics)
• Cell Proliferation
• Cell Survival (genetics)
• Female
• Fibronectins (genetics, metabolism)
• Gene Expression Regulation, Neoplastic
• Humans
• Neoplasms, Glandular and Epithelial (genetics, metabolism, pathology)
• Ovarian Neoplasms (genetics, metabolism, pathology)
• RNA Interference
• Reverse Transcriptase Polymerase Chain Reaction
• Thrombomodulin (genetics, metabolism)
• Vimentin (genetics, metabolism)