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

Research output: Contribution to journalArticle

Abstract

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
JournalHepatology
DOIs
Publication statusE-pub ahead of print - Jul 12 2019

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Catenins
Focal Adhesion Protein-Tyrosine Kinases
Epigenomics
Androgen Receptors
M Phase Cell Cycle Checkpoints
Adipogenesis
Liver
Oxidative Phosphorylation
Genes
Homeostasis
Transcription Factors
Fatty Acids
Cholesterol
Mutation

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FAK/CAT network may act as a regulator of HCC epigenetics. / Romito, Ilaria; Panera, Nadia; D'Ermo, Giuseppe; Alisi, Anna.

In: Hepatology, 12.07.2019.

Research output: Contribution to journalArticle

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title = "FAK/CAT network may act as a regulator of HCC epigenetics",
abstract = "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.",
author = "Ilaria Romito and Nadia Panera and Giuseppe D'Ermo and Anna Alisi",
note = "This article is protected by copyright. All rights reserved.",
year = "2019",
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AU - Romito, Ilaria

AU - Panera, Nadia

AU - D'Ermo, Giuseppe

AU - Alisi, Anna

N1 - This article is protected by copyright. All rights reserved.

PY - 2019/7/12

Y1 - 2019/7/12

N2 - 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.

AB - 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.

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