Abstract
Tgf-Beta is a pleiotropic cytokine with diverse functions on hepatic cells. The well-known function of Tgf-Beta in pathogenesis of liver disease is to stimulate liver fibrosis that often precedes the onset of liver cancer. While Tgf-Beta-mediated fibrosis seems to make liver more prone to the development of liver cancer, Tgf-Beta suppresses initial malignant transformation of hepatic cells thru regulation of proliferation and apoptosis. On the other hand, Tgf-Beta has shown to act as an inducer of tumor development thru enhancement of metastatic process. Additionally, it has been shown that Tgf-Beta signaling in hepatocytes promotes hepatocarcinogenesis caused by certain genetic conditions. This review highlights observations that have improved an understanding of how Tgf-Beta contributes to the development of hepatocellular carcinoma.
Highlights
Hepatocellular carcinoma (HCC) is among the most common cancer that causes increasing morbidity and mortality every year (Ferlay et al, 2010; Nordenstedt, White, & El-Serag, 2010)
This review focuses on findings that shed light on mechanism in which Tgf-β influences tumorigenesis of HCC
It was shown that deletion of TβRII in hepatocytes leaded to increased proliferation up-regulation of Cdk2, Cyclin E and Cyclin A expression as well as down-regulation of Cdkn1a/p21 expression in HCC (Baek et al, 2010). These findings indicated tumor-suppressive effect of Tgf-β in the liver during hepatocarcinogenesis
Summary
Hepatocellular carcinoma (HCC) is among the most common cancer that causes increasing morbidity and mortality every year (Ferlay et al, 2010; Nordenstedt, White, & El-Serag, 2010). Chronic injury in diseased livers leads to increased number of reactive cells such as fibrogenic fibroblasts and inflammatory cells. These reactive cells produce various types of potent tropic factor and cytokine that contributes to a malignant transformation of hepatocyte into HCC. The role of Tgf-β appears to favor HCC development in pre-cancerous stage since it promote the accumulation of myofibroblasts and inflammation that are source of inducing factors for malignant transformation.
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