Promotion of growth factor signaling as a critical function of β-catenin during HCC progression

Eunsun Kim, Amanda Lisby, Connie Ma, Nathanael Lo, Ursula Ehmer, Katharina E. Hayer, Emma E. Furth and Patrick Viatour ()
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Eunsun Kim: Center for Childhood Cancer Research
Amanda Lisby: Hospital of the University of Pennsylvania
Connie Ma: Center for Childhood Cancer Research
Nathanael Lo: Center for Childhood Cancer Research
Ursula Ehmer: Technische Universität München
Katharina E. Hayer: Children’s Hospital of Philadelphia
Emma E. Furth: Hospital of the University of Pennsylvania
Patrick Viatour: Center for Childhood Cancer Research

Nature Communications, 2019, vol. 10, issue 1, 1-17

Abstract: Abstract Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. β-catenin is widely thought to be a major oncogene in HCC based on the frequency of mutations associated with aberrant Wnt signaling in HCC patients. Challenging this model, our data reveal that β-catenin nuclear accumulation is restricted to the late stage of the disease. Until then, β-catenin is primarily located at the plasma membrane in complex with multiple cadherin family members where it drives tumor cell survival by enhancing the signaling of growth factor receptors such as EGFR. Therefore, our study reveals the evolving nature of β-catenin in HCC to establish it as a compound tumor promoter during the progression of the disease.

Date: 2019
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DOI: 10.1038/s41467-019-09780-z

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