β-Catenin signaling in hepatocellular carcinoma.

Abstract

Deregulated Wnt/β-catenin signaling is one of the main genetic alterations in human hepatocellular carcinoma (HCC). Comprehensive genomic analyses have revealed that gain-of-function mutation of CTNNB1, which encodes β-catenin, and loss-of-function mutation of AXIN1 occur in approximately 35% of human HCC samples. Human HCCs with activation of the Wnt/β-catenin pathway demonstrate unique gene expression patterns and pathological features. Activated Wnt/β-catenin synergizes with multiple signaling cascades to drive HCC formation, and it functions through its downstream effectors. Therefore, strategies targeting Wnt/β-catenin have been pursued as possible therapeutics against HCC. Here, we review the genetic alterations and oncogenic roles of aberrant Wnt/β-catenin signaling during hepatocarcinogenesis. In addition, we discuss the implication of this pathway in HCC diagnosis, classification, and personalized treatment.

• Authors: Chuanrui Xu, Zhong Xu, Yi Zhang, Matthias Evert, Diego F Calvisi, Xin Chen
• Journal: The Journal of clinical investigation (J Clin Invest) Vol. 132 Issue 4 (02 15 2022) ISSN: 1558-8238 [Electronic] United States
• PMID: 35166233 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)

Chemical References

• AXIN1 protein, human
• Axin Protein
• CTNNB1 protein, human
• Neoplasm Proteins
• beta Catenin

Topics

• Axin Protein (genetics, metabolism)
• Carcinoma, Hepatocellular (genetics, metabolism)
• Humans
• Liver Neoplasms (genetics, metabolism)
• Neoplasm Proteins (genetics, metabolism)
• Wnt Signaling Pathway
• beta Catenin (genetics, metabolism)