Τίτλος:
Histone deacetylase inhibitors in the treatment of hepatocellular carcinoma: Current evidence and future opportunities
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Hepatocellular carcinoma (HCC) remains a major health problem worldwide with a continuous increasing prevalence. Despite the introduction of targeted therapies like the multi-kinase inhibitor sorafenib, treatment outcomes are not encouraging. The prognosis of advanced HCC is still dismal, underlying the need for novel effective treatments. Apart from the various risk factors that predispose to the development of HCC, epigenetic factors also play a functional role in tumor genesis. Histone deacetylases (HDACs) are enzymes that remove acetyl groups from histone lysine residues of proteins, such as the core nucleosome histones, in this way not permitting DNA to loosen from the histone octamer and consequently preventing its transcription. Considering that HDAC activity is reported to be up-regulated in HCC, treatment strategies with HDAC inhibitors (HDACIs) showed some promising results. This review focuses on the use of HDACIs as novel anticancer agents and explains the mechanisms of their therapeutic effects in HCC. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
Συγγραφείς:
Garmpis, N.
Damaskos, C.
Garmpi, A.
Georgakopoulou, V.E.
Sarantis, P.
Antoniou, E.A.
Karamouzis, M.V.
Nonni, A.
Schizas, D.
Diamantis, E.
Koustas, E.
Farmaki, P.
Syllaios, A.
Patsouras, A.
Kontzoglou, K.
Trakas, N.
Dimitroulis, D.
Περιοδικό:
International Journal of Person-Centered Medicine
Λέξεις-κλειδιά:
belinostat; benzamide; biological marker; cyclin dependent kinase; cyclopeptide; histone; histone acetyltransferase; histone deacetylase inhibitor; panobinostat; quisinostat; resminostat; romidepsin; sorafenib; trichostatin A; valproic acid, angiogenesis; antigen presenting cell; antineoplastic activity; apoptosis; cancer prognosis; cancer therapy; carcinogenesis; cell death; cell proliferation; chromatin structure; DNA damage; DNA repair; epigenetics; epithelial mesenchymal transition; gene control; gene expression; genetic transcription; gluconeogenesis; human; immune response; liver cell carcinoma; liver transplantation; microarray analysis; molecularly targeted therapy; nonhuman; nuclear reprogramming; nucleosome; protein expression; radiosensitization; Review; risk factor; signal transduction; tumor growth; tumor suppressor gene; tumor volume; ubiquitination
