TGF-β and hepatocellular carcinoma: When a friend becomes an enemy

Marco Arrese, Alejandra Hernandez, Luis Astete, Lisbell Estrada, Claudio Cabello-Verrugio, Daniel Cabrera*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

23 Scopus citations


Hepatocellular carcinoma (HCC) is the third most common cause of cancer death worldwide accounting for more than 700 thousand deaths per year. Most of the HCC develops in a cirrhotic liver, a microenvironment where fibrotic tissue replaces parenchymal cells. Thus, there is a close connection between fibrosis and HCC development. Understanding the cellular and molecular mechanisms involved in this process is a crucial step to advance in novel therapeutic or pharmacological strategies to prevent or improve the course of this malignancy. A key molecular player capable of modulating cell growth and fibrosis is the Transforming Growth Factor-beta (TGF-β). Interestingly, TGF-β seems to act like a switch, since it has dual and opposite roles during early and late phases of cancer development. Therefore to develop therapies that target TGF-β signaling pathway for HCC treatment is important to understand the underlying pathogenetic mechanisms at play with special emphasis in the crosstalk between TGF-β and other signaling pathways. In recent years, a plethora of TGR-β have been developed and some of them are under clinical investigations for testing in patients with advanced HCC. In this review, we summarize recent knowledge about the role of TGF-β signaling pathway in HCC progression.

Original languageEnglish
Pages (from-to)1172-1179
Number of pages8
JournalCurrent Protein and Peptide Science
Issue number12
StatePublished - 2018
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2018 Bentham Science Publishers.


  • Cirrhosis
  • HCC
  • Hepatocellular carcinoma
  • Liver cancer
  • Pathogenesis
  • TGF-β


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