NF-κB in liver cancer: The plot thickens

Shlomi Finkin, Eli Pikarsky*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

9 Scopus citations


The role of the NF-κB signaling pathway in liver cancer is complex. While some evidence suggests that in the liver, like in many other organ systems, NF-κB is oncogenic, there is strong evidence showing that in certain liver cancer models NF-κB suppresses tumorigenesis. These contrasting findings cannot be dismissed on technicalities and are likely due to the complex nature of the NF-κB response. Similar contrasting findings regarding NF-κB activity are revealed in skin cancer models. Thus, it is possible that the contradictory role of NF-κB in tumorigenesis is a general phenomenon and not an oddity related solely to the liver. Further studies are indicated to decipher the underlying molecular mechanisms. Revealing these mechanisms may facilitate the identification of patient subgroups and specific situations in which NF-κB inhibition will be a preferred therapeutic option. Moreover, it is possible that specific interventions could boost the tumor suppressor functions of NF-κB in tumors that harbor mutations that render this pathway constitutively active.

Original languageAmerican English
Title of host publicationNF-kB in Health and Disease
Number of pages12
StatePublished - 2011

Publication series

NameCurrent Topics in Microbiology and Immunology
ISSN (Print)0070-217X

Bibliographical note

Funding Information:
We are grateful to members of our lab as well as Dr. Yinon Ben-Neriah and members of his lab for continuous fruitful discussions. Work in the laboratory of Eli Pikarsky is supported by grants from the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, the Israel Science Foundation, the Israel Cancer Research Fund, the DKFZ MOST collaboration, and the Ministry of Health.


Dive into the research topics of 'NF-κB in liver cancer: The plot thickens'. Together they form a unique fingerprint.

Cite this