FAK/CAT network may act as a regulator of HCC epigenetics

Ilaria Romito, Nadia Panera, Giuseppe D'Ermo, Anna Alisi

Research output: Contribution to journalArticlepeer-review


We read with interest the very valuable article recently published by Na and colleagues [1] that deciphered the crucial role of focal adhesion kinase (FAK)/β-catenin (CAT) network in hepatocarcinogenesis. In order to unveil this mechanism the authors overexpressed FAK alone, constitutively active CAT alone, or a combination of both in the livers of C57/BL6 mice. FAK overexpression or CAT mutation were not sufficient to induce HCC, whereas combined FAK/CAT led to hepatocarcinogenesis in mouse. Na et al. [1] also demonstrated that FAK activity was crucial for development of FAK/CAT-dependent HCC. The authors found that many genes closely related to hepatocarcinogenesis were enriched in FAK/CAT-induced HCCs, including genes involved in oxidative phosphorylation, fatty acid metabolism, adipogenesis, mechanistic target of rapamycin complex 1 signaling, G2/M checkpoint, mitotic spindle formation, and cholesterol homeostasis. Interestingly, in the liver samples of FAK/CAT mice the authors revealed a significant increase of the CAT binding to the promoter of androgen receptor (AR) respect to the control samples. AR has been previously reported as a direct transcriptional target of CAT/transcription factor 4 [2]. This article is protected by copyright. All rights reserved.

Original languageEnglish
Publication statusE-pub ahead of print - Jul 12 2019


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