Role of Histone-Modifying Enzymes and Their Complexes in Regulation of Chromatin Biology

Biochemistry ◽  
2016 ◽  
Vol 55 (11) ◽  
pp. 1584-1599 ◽  
Author(s):  
Renee DesJarlais ◽  
Peter J. Tummino
Keyword(s):  
Histone Modifying Enzymes ◽  
Chromatin Biology

scholarly journals Histone Modifying Enzymes in Gynaecological Cancers

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 816
Author(s):  
Priya Ramarao-Milne ◽  
Olga Kondrashova ◽  
Sinead Barry ◽  
John D. Hooper ◽  
Jason S. Lee ◽  
...  
Keyword(s):  
Genome Instability ◽  
Cpg Islands ◽  
Gene Promoter ◽  
Driver Mutations ◽  
Promoter Regions ◽  
Post Translational Modifications ◽  
Chromatin Dynamics ◽  
Cancer Types ◽  
Histone Modifying Enzymes

Genetic and epigenetic factors contribute to the development of cancer. Epigenetic dysregulation is common in gynaecological cancers and includes altered methylation at CpG islands in gene promoter regions, global demethylation that leads to genome instability and histone modifications. Histones are a major determinant of chromosomal conformation and stability, and unlike DNA methylation, which is generally associated with gene silencing, are amenable to post-translational modifications that induce facultative chromatin regions, or condensed transcriptionally silent regions that decondense resulting in global alteration of gene expression. In comparison, other components, crucial to the manipulation of chromatin dynamics, such as histone modifying enzymes, are not as well-studied. Inhibitors targeting DNA modifying enzymes, particularly histone modifying enzymes represent a potential cancer treatment. Due to the ability of epigenetic therapies to target multiple pathways simultaneously, tumours with complex mutational landscapes affected by multiple driver mutations may be most amenable to this type of inhibitor. Interrogation of the actionable landscape of different gynaecological cancer types has revealed that some patients have biomarkers which indicate potential sensitivity to epigenetic inhibitors. In this review we describe the role of epigenetics in gynaecological cancers and highlight how it may exploited for treatment.

Epigenetic regulation of adipogenesis by histone-modifying enzymes

Epigenomics ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 235-251
Author(s):  
Paolo E Macchia ◽  
Immacolata C Nettore ◽  
Fabiana Franchini ◽  
Laura Santana-Viera ◽  
Paola Ungaro
Keyword(s):  
Epigenetic Regulation ◽  
Transcriptional Control ◽  
Metabolic Diseases ◽  
Epigenetic Mechanisms ◽  
Differentiation Process ◽  
Histone Tails ◽  
Histone Modifying Enzymes ◽  
Epigenomic Regulation ◽  
Adipocyte Development

Many studies investigating the transcriptional control of adipogenesis have been published so far; recently the research is focusing on the role of epigenetic mechanisms in regulating the process of adipocyte development. Histone-modifying enzymes and the histone tails post-transcriptional modifications catalyzed by them, are fundamentally involved in the epigenetic regulation of adipogenesis. In our review, we will discuss recent advances in epigenomic regulation of adipogenesis with a focus on histone-modifying enzymes implicated in the various phases of adipocytes differentiation process from mesenchymal stem cells to mature adipocytes. Understanding adipogenesis, may provide new ways to treat obesity and related metabolic diseases.

scholarly journals LSD1, a double-edged sword, confers dynamic chromatin regulation but commonly promotes aberrant cell growth

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 2016 ◽  
Author(s):  
Meghan M Kozub ◽  
Ryan M Carr ◽  
Gwen L Lomberk ◽  
Martin E Fernandez-Zapico
Keyword(s):  
Gene Expression ◽  
Chromatin Remodeling ◽  
Cellular Differentiation ◽  
Critical Role ◽  
Histone Demethylase ◽  
Epigenetic Changes ◽  
Lysine Specific Demethylase ◽  
Wide Range ◽  
Histone Modifying Enzymes

Histone-modifying enzymes play a critical role in chromatin remodeling and are essential for influencing several genome processes such as gene expression and DNA repair, replication, and recombination. The discovery of lysine-specific demethylase 1 (LSD1), the first identified histone demethylase, dramatically revolutionized research in the field of epigenetics. LSD1 plays a pivotal role in a wide range of biological operations, including development, cellular differentiation, embryonic pluripotency, and disease (for example, cancer). This mini-review focuses on the role of LSD1 in chromatin regulatory complexes, its involvement in epigenetic changes throughout development, and its importance in physiological and pathological processes.

scholarly journals Running Against the Wnt: How Wnt/β-Catenin Suppresses Adipogenesis

2021 ◽  
Vol 9 ◽  
Author(s):  
Twan J. J. de Winter ◽  
Roeland Nusse
Keyword(s):  
Wnt Signaling ◽  
Adipocyte Differentiation ◽  
Metabolic Diseases ◽  
Cell Mass ◽  
Terminal Differentiation ◽  
Precursor Cell ◽  
Main Role ◽  
Histone Modifying Enzymes ◽  
Wnt Inhibitors

Mesenchymal stem cells (MSCs) give rise to adipocytes, osteocytes, and chondrocytes and reside in various tissues, including bone marrow and adipose tissue. The differentiation choices of MSCs are controlled by several signaling pathways, including the Wnt/β-catenin signaling. When MSCs undergo adipogenesis, they first differentiate into preadipocytes, a proliferative adipocyte precursor cell, after which they undergo terminal differentiation into mature adipocytes. These two steps are controlled by the Wnt/β-catenin pathway, in such a way that when signaling is abrogated, the next step in adipocyte differentiation can start. This sequence suggests that the main role of Wnt/β-catenin signaling is to suppress differentiation while increasing MSC and preadipocytes cell mass. During later steps of MSC differentiation, however, active Wnt signaling can promote osteogenesis instead of keeping the MSCs undifferentiated and proliferative. The exact mechanisms behind the various functions of Wnt signaling remain elusive, although recent research has revealed that during lineage commitment of MSCs into preadipocytes, Wnt signaling is inactivated by endogenous Wnt inhibitors. In part, this process is regulated by histone-modifying enzymes, which can lead to increased or decreased Wnt gene expression. The role of Wnt in adipogenesis, as well as in osteogenesis, has implications for metabolic diseases since Wnt signaling may serve as a therapeutic target.

scholarly journals Evolution of Epigenome as the Blueprint for Carcinogenesis

2021 ◽  
Author(s):  
Zeenat Farooq ◽  
Ambreen Shah ◽  
Mohammad Tauseef ◽  
Riyaz A. Rather ◽  
Mumtaz Anwar
Keyword(s):  
Dna Methylation ◽  
Cancer Research ◽  
Dna Sequence ◽  
Cancer Type ◽  
Epigenetic Mechanisms ◽  
Respective Role ◽  
Non Coding Rnas ◽  
Chromatin Biology ◽  
Epigenetic Signatures

Epigenetics “above or over genetics” is the term used for processes that result in modifications which are stably inherited through cell generations, without changing the underlying DNA sequence of the cell. These include DNA methylation, Post-translational histone modification and non-coding RNAs. Over the last two decades, interest in the field of epigenetics has grown manifold because of the realization of its involvement in key cellular and pathological processes beyond what was initially anticipated. Epigenetics and chromatin biology have been underscored to play key roles in diseases like cancer. The landscape of different epigenetic signatures can vary considerably from one cancer type to another, and even from one ethnic group to another in the case of same cancer. This chapter discusses the emerging role of epigenetics and chromatin biology in the field of cancer research. It discusses about the different forms of epigenetic mechanisms and their respective role in carcinogenesis in the light of emerging research.

scholarly journals The Role of DNA/Histone Modifying Enzymes and Chromatin Remodeling Complexes in Testicular Germ Cell Tumors

Cancers ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 6 ◽  
Author(s):  
João Lobo ◽  
Rui Henrique ◽  
Carmen Jerónimo
Keyword(s):  
Germ Cell ◽  
Germ Cell Tumors ◽  
In Silico Analysis ◽  
Dna Methyltransferases ◽  
The Cancer Genome Atlas ◽  
Testicular Germ Cell Tumors ◽  
Testicular Germ Cell ◽  
Chromatin Remodelers ◽  
Histone Modifying Enzymes

It is well established that cancer cells exhibit alterations in chromatin structure and accessibility. Indeed, the dysregulation of many protein-coding players with enzymatic activity (DNA and histone-modifying enzymes) and chromatin remodelers have been depicted in various tumor models in recent years. Still, little attention has been directed towards testicular germ cell tumors (TGCTs)—representing the most common neoplasm among young adult Caucasian men—with most studies focusing on exploring the role of DNA methyltransferases (DNMTs) and DNA demethylases (TETs). TGCTs represent a complex tumor model, associated with developmental and embryogenesis-related phenomena, and display seldom (cyto)genetic aberrations, leaving room for Epigenetics to explain such morphological and clinical diversity. Herein, we have summarized the major findings that were reported in literature regarding the dysregulation of DNA/histone-modifying enzymes and chromatin remodelers in TGCTs. Additionally, we performed in silico analysis of The Cancer Genome Atlas database to find the most relevant of those players in TGCTs. We concluded that several DNA/histone-modifying enzymes and chromatin remodelers may serve as biomarkers for subtyping, dictating prognosis and survival, and, possibly, for serving as targets of directed, less toxic therapies.

scholarly journals Atherogenic Factors and Their Epigenetic Relationships

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Ana Z. Fernandez ◽  
Andrew L. Siebel ◽  
Assam El-Osta
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Dna Methylation ◽  
Smooth Muscle ◽  
Immune Cells ◽  
Human Disease ◽  
Physiology And Biochemistry ◽  
Histone Modifying Enzymes ◽  
Atherosclerotic Process

Hypercholesterolemia, homocysteine, oxidative stress, and hyperglycemia have been recognized as the major risk factors for atherogenesis. Their impact on the physiology and biochemistry of vascular cells has been widely demonstrated for the last century. However, the recent discovery of the role of epigenetics in human disease has opened up a new field in the study of atherogenic factors. Thus, epigenetic tags in endothelial, smooth muscle, and immune cells seem to be differentially affected by similar atherogenic stimuli. This paper summarizes some recent works on expression of histone-modifying enzymes and DNA methylation directly linked to the presence of risk factors that could lead to the development or prevention of the atherosclerotic process.

scholarly journals Epi-miRNAs: Regulators of the Histone Modification Machinery in Human Cancer

2022 ◽  
Vol 2022 ◽  
pp. 1-22
Author(s):  
Deniz Mortazavi ◽  
Behnoush Sohrabi ◽  
Meysam Mosallaei ◽  
Ziba Nariman-Saleh-Fam ◽  
Milad Bastami ◽  
...  
Keyword(s):  
Histone Modification ◽  
Cell Fate ◽  
Target Genes ◽  
Human Cancer ◽  
Noncoding Rnas ◽  
Fine Tuning ◽  
Small Noncoding Rnas ◽  
Histone Modifiers ◽  
Histone Modifying Enzymes

Cancer is a leading cause of death and disability worldwide. Epigenetic deregulation is one of the most critical mechanisms in carcinogenesis and can be classified into effects on DNA methylation and histone modification. MicroRNAs are small noncoding RNAs involved in fine-tuning their target genes after transcription. Various microRNAs control the expression of histone modifiers and are involved in a variety of cancers. Therefore, overexpression or downregulation of microRNAs can alter cell fate and cause malignancies. In this review, we discuss the role of microRNAs in regulating the histone modification machinery in various cancers, with a focus on the histone-modifying enzymes such as acetylases, deacetylases, methyltransferases, demethylases, kinases, phosphatases, desumoylases, ubiquitinases, and deubiquitinases. Understanding of microRNA-related aberrations underlying histone modifiers in pathogenesis of different cancers can help identify novel therapeutic targets or early detection approaches that allow better management of patients or monitoring of treatment response.

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