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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

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Knockdown of thrombomodulin enhances HCC cell migration through increase of ZEB1 and decrease of E-cadherin gene

Ming-Te Huang¹, Po-Li Wei, Jun-Jen Liu

¹Department of Surgery, Taipei Medical University, Taipei City, Taiwan.

Annals of Surgical Oncology

|July 14, 2010

Summary

Thrombomodulin (TM) downregulation enhances hepatocellular carcinoma (HCC) cell metastasis by increasing ZEB1 and decreasing E-cadherin. TM may be a key regulator of HCC progression and metastasis.

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Area of Science:

Oncology
Molecular Biology
Cell Biology

Background:

Thrombomodulin (TM) is crucial for circulation homeostasis.
Decreased TM expression is linked to cancer metastasis in various tissues.
The role of TM in hepatocellular carcinoma (HCC) progression remains largely unknown.

Purpose of the Study:

To investigate the role of Thrombomodulin (TM) in hepatocellular carcinoma (HCC) metastasis.
To elucidate the molecular mechanisms by which TM influences HCC cell migration.

Main Methods:

Characterized TM expression in HCC cell lines (HepJ5, skHep-1) using real-time PCR and Western blotting.
Manipulated TM expression via shRNA knockdown and overexpression.
Assessed HCC cell migratory ability using Transwell migration assays.

Main Results:

TM was highly expressed in skHep-1 HCC cells.
Silencing TM in skHep-1 cells significantly increased metastatic capability.
Overexpressing TM in HepJ5 cells decreased metastatic ability.
Decreased TM-mediated cell migration was linked to ZEB1 upregulation and E-cadherin downregulation.

Conclusions:

Thrombomodulin (TM) acts as a modulator of cancer metastasis in HCC.
Downregulation of TM in HCC may promote metastasis through increased ZEB1 and decreased E-cadherin expression.