Hepatocellular carcinoma is one of the most common malignant tumor and leading cause of death worldwide. Tumor genes, signals from tumor stroma, recruited inflammatory cells and hypoxia has been reported to switch on angiogenesis. Vascular endothelial growth factor is a pleiotropic factor that regulates cell proliferation, vascular permeability and plays an important role in tumor angiogenesis through its different angiogenic receptors. Multifunctional regulatory cytokine transforming growth factor-β also controls cell proliferation, differentiation, extracellular matrix production and survival/or apoptosis of many types cells. By raising level of epithelialmesenchymal transition, transforming growth factor-β creates a favourable microenvironment for tumor cell growth. Depending upon the stage of cancer progression it can either initiate tumor development, progression and metastasis or can act as a tumor suppressor. In the present review, an attempt has been made to comprehensively define the role of Vascular Endothelial Growth Factor and transforming growth factor-β in the development and progression of hepatocellular carcinoma.
Key words: Hepatocellular carcinoma; VEGF; TGF-β; angiogenesis; cancer
scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.
The articles in Bibliomed are open access articles licensed under Creative Commons Attribution 4.0 International License (CC BY), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
We use cookies and other tracking technologies to work properly, to analyze our website traffic, and to understand where our visitors are coming from. More InfoGot It!