Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Due to the high incidence of post-operative recurrence after current treatments, the identification of new and more effective drugs is required. In previous years, new targetable genes/pathways involved in HCC pathogenesis have been discovered through the help of high-throughput sequencing technologies. Mutations in TP53 and β-catenin genes are the most frequent aberrations in HCC. However, approaches able to reverse the effect of these mutations might be unpredictable. In fact, if the reactivation of proteins, such as p53 in tumours, holds great promise as anticancer therapy, there are studies arguing that chronic activation of these types of molecules may be deleterious. Thus, recently the efforts on potential targets have focused on actionable mutations, such as those occurring in the gene encoding for focal adhesion kinase (FAK). This tyrosine kinase, localized to cellular focal contacts, is over-expressed in a variety of human tumours, including HCC. Moreover, several lines of evidence demonstrated that FAK depletion or inhibition impair in vitro and in vivo HCC growth and metastasis. Here, we provide an overview of FAK expression and activity in the context of tumour biology, discussing the current evidence of its connection with HCC development and progression.

Focal adhesion kinase: Insight into molecular roles and functions in hepatocellular carcinoma / Panera, Nadia; Crudele, Annalisa; Romito, Ilaria; Gnani, Daniela; Alisi, Anna. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1661-6596. - 18:1(2017), pp. 1-16. [10.3390/ijms18010099]

Focal adhesion kinase: Insight into molecular roles and functions in hepatocellular carcinoma

Panera, Nadia;Romito, Ilaria;Alisi, Anna
2017

Abstract

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Due to the high incidence of post-operative recurrence after current treatments, the identification of new and more effective drugs is required. In previous years, new targetable genes/pathways involved in HCC pathogenesis have been discovered through the help of high-throughput sequencing technologies. Mutations in TP53 and β-catenin genes are the most frequent aberrations in HCC. However, approaches able to reverse the effect of these mutations might be unpredictable. In fact, if the reactivation of proteins, such as p53 in tumours, holds great promise as anticancer therapy, there are studies arguing that chronic activation of these types of molecules may be deleterious. Thus, recently the efforts on potential targets have focused on actionable mutations, such as those occurring in the gene encoding for focal adhesion kinase (FAK). This tyrosine kinase, localized to cellular focal contacts, is over-expressed in a variety of human tumours, including HCC. Moreover, several lines of evidence demonstrated that FAK depletion or inhibition impair in vitro and in vivo HCC growth and metastasis. Here, we provide an overview of FAK expression and activity in the context of tumour biology, discussing the current evidence of its connection with HCC development and progression.
2017
Cancer stem cells; Focal adhesion kinase; Hepatocellular carcinoma; Metastasis; Proliferation; Carcinoma, Hepatocellular; Disease Progression; Focal Adhesion Protein-Tyrosine Kinases; Humans; Liver Neoplasms; Models, Genetic; Neoplasm Invasiveness; Neoplastic Stem Cells; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic Chemistry
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Focal adhesion kinase: Insight into molecular roles and functions in hepatocellular carcinoma / Panera, Nadia; Crudele, Annalisa; Romito, Ilaria; Gnani, Daniela; Alisi, Anna. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1661-6596. - 18:1(2017), pp. 1-16. [10.3390/ijms18010099]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1026465
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