scholarly journals Histone Deacetylase Inhibitors in Programmed Cell Death and Cancer Therapy

Cell Cycle ◽  
2005 ◽  
Vol 4 (4) ◽  
pp. 549-551 ◽  
Author(s):  
Paul A. Marks ◽  
Xuejun Jiang
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Programmed Cell Death ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors

scholarly journals Epigenetic Targeting of Autophagy via HDAC Inhibition in Tumor Cells: Role of p53

2018 ◽  
Vol 19 (12) ◽  
pp. 3952 ◽  
Author(s):  
Maria Mrakovcic ◽  
Lauren Bohner ◽  
Marcel Hanisch ◽  
Leopold F. Fröhlich
Keyword(s):  
Cell Death ◽  
Tumor Cells ◽  
Histone Deacetylase ◽  
Stress Responses ◽  
Histone Deacetylase Inhibitors ◽  
Tumor Therapy ◽  
Regulatory System ◽  
Anticancer Activities ◽  
Mutational Status

Tumor development and progression is the consequence of genetic as well as epigenetic alterations of the cell. As part of the epigenetic regulatory system, histone acetyltransferases (HATs) and deacetylases (HDACs) drive the modification of histone as well as non-histone proteins. Derailed acetylation-mediated gene expression in cancer due to a delicate imbalance in HDAC expression can be reversed by histone deacetylase inhibitors (HDACi). Histone deacetylase inhibitors have far-reaching anticancer activities that include the induction of cell cycle arrest, the inhibition of angiogenesis, immunomodulatory responses, the inhibition of stress responses, increased generation of oxidative stress, activation of apoptosis, autophagy eliciting cell death, and even the regulation of non-coding RNA expression in malignant tumor cells. However, it remains an ongoing issue how tumor cells determine to respond to HDACi treatment by preferentially undergoing apoptosis or autophagy. In this review, we summarize HDACi-mediated mechanisms of action, particularly with respect to the induction of cell death. There is a keen interest in assessing suitable molecular factors allowing a prognosis of HDACi-mediated treatment. Addressing the results of our recent study, we highlight the role of p53 as a molecular switch driving HDACi-mediated cellular responses towards one of both types of cell death. These findings underline the importance to determine the mutational status of p53 for an effective outcome in HDACi-mediated tumor therapy.

scholarly journals Histone Deacetylase Inhibitors: Synthesis of Tetrapeptide Analogue SAHA/TPX

2011 ◽  
Vol 8 (s1) ◽  
pp. S79-S84
Author(s):  
Lynda Ekou ◽  
Tchirioua Ekou ◽  
Isabelle Opalinski ◽  
Jean Pierre Gesson
Keyword(s):  
Clinical Trial ◽  
Cancer Therapy ◽  
Phase I ◽  
Histone Deacetylase ◽  
Hydroxamic Acid ◽  
Histone Deacetylase Inhibitors ◽  
Hdac Inhibitors ◽  
Growth Arrest ◽  
Suberoylanilide Hydroxamic Acid ◽  
Specific Inhibitors

The inhibition of HDAC (histone deacetylase) activity by specific inhibitors induces growth arrest, differentiation and apoptosis of transformed or several cancer cells. Some of these inhibitors are in clinical trial at phase I or phase II. The discovery and development of specific HDAC inhibitors are helpful for cancer therapy. In this paper we describe the synthesis of simple inhibitorBhybrid analogue suberoylanilide hydroxamic acid (SAHA), trapoxinB(TPX B) in as little as five steps. This compound is interesting lead for the design of potent inhibitors of histone deacetylase.

scholarly journals The Effect of Organoselenium Compounds on Histone Deacetylase Inhibition and Their Potential for Cancer Therapy

2021 ◽  
Vol 22 (23) ◽  
pp. 12952
Author(s):  
Theolan Adimulam ◽  
Thilona Arumugam ◽  
Ashmika Foolchand ◽  
Terisha Ghazi ◽  
Anil A. Chuturgoon
Keyword(s):  
Cancer Therapy ◽  
Histone Deacetylase ◽  
Gene Transcription ◽  
Histone Deacetylase Inhibitors ◽  
Cancer Therapeutics ◽  
Epigenetic Changes ◽  
Organoselenium Compounds ◽  
Histone Proteins ◽  
Acetylation Status ◽  
Natural And Synthetic

Genetic and epigenetic changes alter gene expression, contributing to cancer. Epigenetic changes in cancer arise from alterations in DNA and histone modifications that lead to tumour suppressor gene silencing and the activation of oncogenes. The acetylation status of histones and non-histone proteins are determined by the histone deacetylases and histone acetyltransferases that control gene transcription. Organoselenium compounds have become promising contenders in cancer therapeutics. Apart from their anti-oxidative effects, several natural and synthetic organoselenium compounds and metabolites act as histone deacetylase inhibitors, which influence the acetylation status of histones and non-histone proteins, altering gene transcription. This review aims to summarise the effect of natural and synthetic organoselenium compounds on histone and non-histone protein acetylation/deacetylation in cancer therapy.

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