Endothelial Cell-Derived TGF- β Promotes Epithelial-Mesenchymal Transition via CD133 in HBx-Infected Hepatoma Cells

Conclusion: The study indicates that secretory factors like TGF-β from neighboring endothelial cells may enhance expression of CD133 and impart an aggressive EMT phenotype to HBx-infected hepatoma cells in HBV induced HCC. Introduction Hepatocellular Carcinoma (HCC) is one of the most common cancer worldwide, representing approximately 4% of all malignancies (1). It has been estimated that more than 50% of HCC cases in the world are associated with hepatitis B virus (HBV) (2). HBV is a partially double stranded DNA virus belonging to the Hepadnavirus family. The HBV genome is 3.2 kb in size and contains four overlapping major open reading frames tightly arranged that encode polymerase, surface (HBsAg), core (HBcAg), and X proteins (HBx). HBx, a 17-kd protein is the most frequently integrated viral sequence found in HBV-induced HCCs (3). HBx is known to interact with various transcription factors of the host and affect activation and modulation of several signal transduction pathways (4). The activation of these signal transduction pathways by HBx leads to the upregulation of a number of cellular genes, including those of growth factors and oncogenes. During late stages of tumor progression, HBx also drives the activation of cellular pathways associated with metastasis and angiogenesis, which play an important role in the growth and spread of HCC (5). Many recent studies have now demonstrated that the growth and spread of tumor is not only affected by alterati...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research