Certain biomakers that appear to trigger aggressiveness of liver cancer have been identified by scientists from Taipei Veterans General Hospital.
Hepatocellular carcinoma (HCC) or primary liver cancer forms in the epithelial tissue of the liver and is most commonly caused by the hepatitis B virus (HBV) or hepatitis C virus (HCV).
The researchers investigated the molecular mechanisms of HCC and provided a comprehensive profile of multiple Epithelial-Mesenchymal Transition (EMT) markers.
EMT is critical in the development of invasiveness and metastatic potential of human cancers, and described as process where epithelial cells no longer adhere to one another, taking on fibroblastic properties.
The EMT process is initiated by suppression of E-cadherin function through the major EMT regulators (Snail, Slug, and Twist).
E-cadherin (calcium dependent adhesion molecules) is a type of protein found in the epithelial cells that ensure tissue cells bind together. When E-cadherin function is lost, cancer is able to progress and metastasize.
The study showed that Snail and Twist, but not Slug are the major inducers of EMT in HCC.
During the study, professor Jaw-Ching Wu and colleagues obtained samples of primary HCC with adjacent non-tumorous liver tissues from 123 patients who had hepatic resection surgery. Reduced E-cadherin function was observed in 60.2pct of patients.
"We found a significant decrease in cancer-free intervals and overall survival for those patients who had a reduction in E-cadherin function," said Dr. Wu.
The results show that co-expression Snail and Twist (transcription factors or proteins that control when genes are switched on or off) indicates the worst prognosis for HCC patients.
"Our research is the first to prove that the two proteins (Snail and Twist) work independently, but together promote EMT," said Wu.
The study is published in journal Hepatology.