Journal articles: 'Epigenetic Modulations'

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Kaur, Jasmine, Abdelkader Daoud, and Scott T. Eblen. "Targeting Chromatin Remodeling for Cancer Therapy." Current Molecular Pharmacology 12, no. 3 (July 29, 2019): 215–29. http://dx.doi.org/10.2174/1874467212666190215112915.

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Background: Epigenetic alterations comprise key regulatory events that dynamically alter gene expression and their deregulation is commonly linked to the pathogenesis of various diseases, including cancer. Unlike DNA mutations, epigenetic alterations involve modifications to proteins and nucleic acids that regulate chromatin structure without affecting the underlying DNA sequence, altering the accessibility of the transcriptional machinery to the DNA, thus modulating gene expression. In cancer cells, this often involves the silencing of tumor suppressor genes or the increased expression of genes involved in oncogenesis. Advances in laboratory medicine have made it possible to map critical epigenetic events, including histone modifications and DNA methylation, on a genome-wide scale. Like the identification of genetic mutations, mapping of changes to the epigenetic landscape has increased our understanding of cancer progression. However, in contrast to irreversible genetic mutations, epigenetic modifications are flexible and dynamic, thereby making them promising therapeutic targets. Ongoing studies are evaluating the use of epigenetic drugs in chemotherapy sensitization and immune system modulation. With the preclinical success of drugs that modify epigenetics, along with the FDA approval of epigenetic drugs including the DNA methyltransferase 1 (DNMT1) inhibitor 5-azacitidine and the histone deacetylase (HDAC) inhibitor vorinostat, there has been a rise in the number of drugs that target epigenetic modulators over recent years. Conclusion: We provide an overview of epigenetic modulations, particularly those involved in cancer, and discuss the recent advances in drug development that target these chromatin-modifying events, primarily focusing on novel strategies to regulate the epigenome.

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Wrede, Dylan, Mika Bordak, Yeabtsega Abraham, and Masfique Mehedi. "Pulmonary Pathogen-Induced Epigenetic Modifications." Epigenomes 7, no. 3 (July 6, 2023): 13. http://dx.doi.org/10.3390/epigenomes7030013.

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Epigenetics generally involves genetic control by factors other than our own DNA sequence. Recent research has focused on delineating the mechanisms of two major epigenetic phenomena: DNA methylation and histone modification. As epigenetics involves many cellular processes, it is no surprise that it can also influence disease-associated gene expression. A direct link between respiratory infections, host cell epigenetic regulations, and chronic lung diseases is still unknown. Recent studies have revealed bacterium- or virus-induced epigenetic changes in the host cells. In this review, we focused on respiratory pathogens (viruses, bacteria, and fungi) induced epigenetic modulations (DNA methylation and histone modification) that may contribute to lung disease pathophysiology by promoting host defense or allowing pathogen persistence.

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Arif, K. M. Taufiqul, Esther K. Elliott, Larisa M. Haupt, and Lyn R. Griffiths. "Regulatory Mechanisms of Epigenetic miRNA Relationships in Human Cancer and Potential as Therapeutic Targets." Cancers 12, no. 10 (October 11, 2020): 2922. http://dx.doi.org/10.3390/cancers12102922.

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Initiation and progression of cancer are under both genetic and epigenetic regulation. Epigenetic modifications including alterations in DNA methylation, RNA and histone modifications can lead to microRNA (miRNA) gene dysregulation and malignant cellular transformation and are hereditary and reversible. miRNAs are small non-coding RNAs which regulate the expression of specific target genes through degradation or inhibition of translation of the target mRNA. miRNAs can target epigenetic modifier enzymes involved in epigenetic modulation, establishing a trilateral regulatory “epi–miR–epi” feedback circuit. The intricate association between miRNAs and the epigenetic architecture is an important feature through which to monitor gene expression profiles in cancer. This review summarises the involvement of epigenetically regulated miRNAs and miRNA-mediated epigenetic modulations in various cancers. In addition, the application of bioinformatics tools to study these networks and the use of therapeutic miRNAs for the treatment of cancer are also reviewed. A comprehensive interpretation of these mechanisms and the interwoven bond between miRNAs and epigenetics is crucial for understanding how the human epigenome is maintained, how aberrant miRNA expression can contribute to tumorigenesis and how knowledge of these factors can be translated into diagnostic and therapeutic tool development.

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Wikumpriya, Gunasekara Chathura, Madhuranga Walawedurage Srinith Prabhatha, Jiye Lee, and Chan-Hee Kim. "Epigenetic Modulations for Prevention of Infectious Diseases in Shrimp Aquaculture." Genes 14, no. 9 (August 25, 2023): 1682. http://dx.doi.org/10.3390/genes14091682.

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Aquaculture assumes a pivotal role in meeting the escalating global food demand, and shrimp farming, in particular, holds a significant role in the global economy and food security, providing a rich source of nutrients for human consumption. Nonetheless, the industry faces formidable challenges, primarily attributed to disease outbreaks and the diminishing efficacy of conventional disease management approaches, such as antibiotic usage. Consequently, there is an urgent imperative to explore alternative strategies to ensure the sustainability of the industry. In this context, the field of epigenetics emerges as a promising avenue for combating infectious diseases in shrimp aquaculture. Epigenetic modulations entail chemical alterations in DNA and proteins, orchestrating gene expression patterns without modifying the underlying DNA sequence through DNA methylation, histone modifications, and non-coding RNA molecules. Utilizing epigenetic mechanisms presents an opportunity to enhance immune gene expression and bolster disease resistance in shrimp, thereby contributing to disease management strategies and optimizing shrimp health and productivity. Additionally, the concept of epigenetic inheritability in marine animals holds immense potential for the future of the shrimp farming industry. To this end, this comprehensive review thoroughly explores the dynamics of epigenetic modulations in shrimp aquaculture, with a particular emphasis on its pivotal role in disease management. It conveys the significance of harnessing advantageous epigenetic changes to ensure the long-term viability of shrimp farming while deliberating on the potential consequences of these interventions. Overall, this appraisal highlights the promising trajectory of epigenetic applications, propelling the field toward strengthening sustainability in shrimp aquaculture.

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Hmood, Qammar Shaker. "Harnessing CRISPR-Cas for Targeted Epigenetic Manipulations: a physiological study of Gene Regulation." European Journal of Medical Genetics and Clinical Biology 1, no. 5 (May 10, 2024): 115–29. http://dx.doi.org/10.61796/jmgcb.v1i5.453.

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Genome engineering, epigenome editing, as one of the prominent research techniques, has also become instrumental in discovering the gene expression regulation mechanisms and exploring their physiological correlates in health and pathology. This review summarizes the state-of-the-art CRISPR-Cas strategies that focus on epigenetics modification and projects its utility in molecular physiology of gene regulation. In this course we will delve into how CRISPR-Cas systems interact with epigenetic signals through DNA methylation, histone modifications and accessibility to chromatin. Then we look at the physiological effects of epigenetic modulations in cellular differentiation and development, cellular signal and homeostasis, disease pathogenesis, and therapeutic for application. Issues and perspectives on how epigenome manipulations can revolutionize therapeutics are also emphasized exploring the potential of precision medicine and individualized therapies. Overall, the review stresses the pivotal role of epigenetic modulation in the development of our understanding of gene expressions/mediation and cellular physiology. It also provides some inputs on the potential directions that the field of genetic engineering might take in the future.

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Wong, Belinda Shu Ee, Qidong Hu, and Gyeong Hun Baeg. "Epigenetic modulations in nanoparticle-mediated toxicity." Food and Chemical Toxicology 109 (November 2017): 746–52. http://dx.doi.org/10.1016/j.fct.2017.07.006.

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Stanzione, Rosita, Maria Cotugno, Franca Bianchi, Simona Marchitti, Maurizio Forte, Massimo Volpe, and Speranza Rubattu. "Pathogenesis of Ischemic Stroke: Role of Epigenetic Mechanisms." Genes 11, no. 1 (January 13, 2020): 89. http://dx.doi.org/10.3390/genes11010089.

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Epigenetics is the branch of molecular biology that studies modifications able to change gene expression without altering the DNA sequence. Epigenetic modulations include DNA methylation, histone modifications, and noncoding RNAs. These gene modifications are heritable and modifiable and can be triggered by lifestyle and nutritional factors. In recent years, epigenetic changes have been associated with the pathogenesis of several diseases such as diabetes, obesity, renal pathology, and different types of cancer. They have also been related with the pathogenesis of cardiovascular diseases including ischemic stroke. Importantly, since epigenetic modifications are reversible processes they could assist with the development of new therapeutic approaches for the treatment of human diseases. In the present review article, we aim to collect the most recent evidence concerning the impact of epigenetic modifications on the pathogenesis of ischemic stroke in both animal models and humans.

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Salinas, Irving, Niharika Sinha, and Aritro Sen. "Androgen-induced epigenetic modulations in the ovary." Journal of Endocrinology 249, no. 3 (June 2021): R53—R64. http://dx.doi.org/10.1530/joe-20-0578.

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In recent years, androgens have emerged as critical regulators of female reproduction and women’s health in general. While high levels of androgens in women are associated with polycystic ovary syndrome (PCOS), recent evidence suggests that a certain amount of direct androgen action through androgen receptor is also essential for normal ovarian function. Moreover, prenatal androgen exposure has been reported to cause developmental reprogramming of the fetus that manifests into adult pathologies, supporting the Developmental Origins of Health and Disease (DOHaD) hypothesis. Therefore, it has become imperative to understand the underlying mechanism of androgen actions and its downstream effects under normal and pathophysiological conditions. Over the years, there has been a lot of studies on androgen receptor function as a transcriptional regulator in the nucleus as well as androgen-induced rapid extra-nuclear signaling. Conversely, new evidence suggests that androgen actions may also be mediated through epigenetic modulation involving both the nuclear and extra-nuclear androgen signaling. This review focuses on androgen-induced epigenetic modifications in female reproduction, specifically in the ovary, and discusses emerging concepts, latest perceptions, and highlight the areas that need further investigation.

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Hoffman, Jessie B., Michael C. Petriello, and Bernhard Hennig. "Impact of nutrition on pollutant toxicity: an update with new insights into epigenetic regulation." Reviews on Environmental Health 32, no. 1-2 (March 1, 2017): 65–72. http://dx.doi.org/10.1515/reveh-2016-0041.

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Abstract Exposure to environmental pollutants is a global health problem and is associated with the development of many chronic diseases, including cardiovascular disease, diabetes and metabolic syndrome. There is a growing body of evidence that nutrition can both positively and negatively modulate the toxic effects of pollutant exposure. Diets high in proinflammatory fats, such as linoleic acid, can exacerbate pollutant toxicity, whereas diets rich in bioactive and anti-inflammatory food components, including omega-3 fatty acids and polyphenols, can attenuate toxicant-associated inflammation. Previously, researchers have elucidated direct mechanisms of nutritional modulation, including alteration of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, but recently, increased focus has been given to the ways in which nutrition and pollutants affect epigenetics. Nutrition has been demonstrated to modulate epigenetic markers that have been linked either to increased disease risks or to protection against diseases. Overnutrition (i.e. obesity) and undernutrition (i.e. famine) have been observed to alter prenatal epigenetic tags that may increase the risk of offspring developing disease later in life. Conversely, bioactive food components, including curcumin, have been shown to alter epigenetic markers that suppress the activation of NF-κB, thus reducing inflammatory responses. Exposure to pollutants also alters epigenetic markers and may contribute to inflammation and disease. It has been demonstrated that pollutants, via epigenetic modulations, can increase the activation of NF-κB and upregulate microRNAs associated with inflammation, cardiac injury and oxidative damage. Importantly, recent evidence suggests that nutritional components, including epigallocatechin gallate (EGCG), can protect against pollutant-induced inflammation through epigenetic regulation of proinflammatory target genes of NF-κB. Further research is needed to better understand how nutrition can modulate pollutant toxicity through epigenetic regulation. Therefore, the objective of this review is to elucidate the current evidence linking epigenetic changes to pollutant-induced diseases and how this regulation may be modulated by nutrients allowing for the development of future personalized lifestyle interventions.

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Pan, Desi, and Xianping Lu. "New therapeutic avenue of epigenetic modulations in cancer." Translational Breast Cancer Research 1 (April 2020): 2. http://dx.doi.org/10.21037/tbcr.2020.03.03.

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Ramesha, K. P., N. Chandra Mohana, B. R. Nuthan, D. Rakshith, and S. Satish. "Epigenetic modulations of mycoendophytes for novel bioactive molecules." Biocatalysis and Agricultural Biotechnology 16 (October 2018): 663–68. http://dx.doi.org/10.1016/j.bcab.2018.09.025.

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Saldanha, Sabita N., and Trygve O. Tollefsbol. "Pathway Modulations and Epigenetic Alterations in Ovarian Tumorbiogenesis." Journal of Cellular Physiology 229, no. 4 (December 17, 2013): 393–406. http://dx.doi.org/10.1002/jcp.24466.

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Santos, Francisco, Hashum Sum, Denise Cheuk Lee Yan, and Alison C. Brewer. "Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis." Cells 14, no. 5 (March 5, 2025): 378. https://doi.org/10.3390/cells14050378.

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Endothelial dysfunction is the main initiating factor in atherosclerosis. Through mechanotransduction, shear stress regulates endothelial cell function in both homeostatic and diseased states. Accumulating evidence reveals that epigenetic changes play critical roles in the etiology of cardiovascular diseases, including atherosclerosis. The metabolic regulation of epigenetics has emerged as an important factor in the control of gene expression in diseased states, but to the best of our knowledge, this connection remains largely unexplored in endothelial dysfunction and atherosclerosis. In this review, we (1) summarize how shear stress (or flow) regulates endothelial (dys)function; (2) explore the epigenetic alterations that occur in the endothelium in response to disturbed flow; (3) review endothelial cell metabolism under different shear stress conditions; and (4) suggest mechanisms which may link this altered metabolism to the regulation of the endothelial epigenome by modulations in metabolite availability. We believe that metabolic regulation plays an important role in endothelial epigenetic reprogramming and could pave the way for novel metabolism-based therapeutic strategies.

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Ge, R., Z. Wang, R. Montironi, Z. Jiang, M. Cheng, M. Santoni, K. Huang, et al. "Epigenetic modulations and lineage plasticity in advanced prostate cancer." Annals of Oncology 31, no. 4 (April 2020): 470–79. http://dx.doi.org/10.1016/j.annonc.2020.02.002.

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Elgazzaz, Mona, and Eric Lazartigues. "Epigenetic modifications of the renin–angiotensin system in cardiometabolic diseases." Clinical Science 135, no. 1 (January 2021): 127–42. http://dx.doi.org/10.1042/cs20201287.

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Abstract Cardiometabolic diseases (CMDs) are among the most prevalent and the highest mortality diseases. Single disease etiology such as gene mutation, polymorphisms, or environmental exposure has failed to explain the origin of CMD. This can be evident in the discrepancies in disease susceptibility among individuals exposed to the same environmental insult or who acquire the same genetic variation. Epigenetics is the intertwining of genetic and environmental factors that results in diversity in the disease course, severity, and prognosis among individuals. Environmental exposures modify the epigenome and thus provide a link for translating environmental impact on changes in gene expression and precipitation to pathological conditions. Renin–angiotensin system (RAS) is comprising genes responsible for the regulation of cardiovascular, metabolic, and glycemic functions. Epigenetic modifications of RAS genes can lead to overactivity of the system, increased sympathetic activity and autonomic dysfunction ultimately contributing to the development of CMD. In this review, we describe the three common epigenetic modulations targeting RAS components and their impact on the susceptibility to cardiometabolic dysfunction. Additionally, we highlight the therapeutic efforts of targeting these epigenetic imprints to the RAS and its effects.

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Abi Zamer, Batoul, Wafaa Abumustafa, Mawieh Hamad, Azzam A. Maghazachi, and Jibran Sualeh Muhammad. "Genetic Mutations and Non-Coding RNA-Based Epigenetic Alterations Mediating the Warburg Effect in Colorectal Carcinogenesis." Biology 10, no. 9 (August 30, 2021): 847. http://dx.doi.org/10.3390/biology10090847.

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Colorectal cancer (CRC) development is a gradual process defined by the accumulation of numerous genetic mutations and epigenetic alterations leading to the adenoma-carcinoma sequence. Despite significant advances in the diagnosis and treatment of CRC, it continues to be a leading cause of cancer-related deaths worldwide. Even in the presence of oxygen, CRC cells bypass oxidative phosphorylation to produce metabolites that enable them to proliferate and survive—a phenomenon known as the “Warburg effect”. Understanding the complex glucose metabolism in CRC cells may support the development of new diagnostic and therapeutic approaches. Here we discuss the most recent findings on genetic mutations and epigenetic modulations that may positively or negatively regulate the Warburg effect in CRC cells. We focus on the non-coding RNA (ncRNA)-based epigenetics, and we present a perspective on the therapeutic relevance of critical molecules and ncRNAs mediating the Warburg effect in CRC cells. All the relevant studies were identified and assessed according to the genes and enzymes mediating the Warburg effect. The findings summarized in this review should provide a better understanding of the relevance of genetic mutations and the ncRNA-based epigenetic alterations to CRC pathogenesis to help overcome chemoresistance.

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Sharda, Sonal, Yvonne Baumer, Alina P. Pang, Abhinav Saurabh, Billy S. Collins, Valerie M. Mitchell, Michael J. Corley, and Tiffany M. Powell-Wiley. "Abstract 2163: Socioeconomic status associates with epigenetic modulation of TET2: An emerging pathway in cardio-oncology." Cancer Research 84, no. 6_Supplement (March 22, 2024): 2163. http://dx.doi.org/10.1158/1538-7445.am2024-2163.

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Abstract Introduction: Adverse social determinants of health (SDOH) are known to accelerate poor outcomes in cardiovascular disease (CVD) and cancer. Clonal Hematopoiesis (CH) is a mechanism implicated in these disease states, partially driven by epigenetic regulatory genes, including TET2. Yet, there is not much known about how epigenetic modulations of TET2 itself may relate to the immune system and subsequent disease development. Hypothesis: We hypothesize that socioeconomic status (SES), as a SDOH marker, relates to epigenetic modulation of TET2. Methods: 60 African American adults (93.3% female, mean age 61) with CVD risk, living in the Washington, D.C. area self-reported their SES as household income. Immune system activity was assessed via splenic activity (SpleenA) by 18FDG PET/CT. Serum cytokine levels were measured by ELISA and DNA methylation analysis evaluated the epigenetic modulations of TET2. Multivariable regression analysis adjusted for ASCVD 10-year risk score and BMI was used to examine associations. Results: Out of 33 TET2 methylation sites, we found 3 sites that were significantly related to SES. Notably, only Tet2cg09666717 (SES β=0.310, p=0.038) was also associated with SpleenA (β=-0.453, p=0.036) and several cytokines: IL-17A, IL-1β and TNFα along with trending to significance with IFN-γ (Table). Conclusion: Thus, we found that SES associates with hypomethylation of Tet2cg09666717, which further related to SpleenA and inflammatory markers. Our findings are hypothesis generating and suggest that lower SES may relate to inflammation and immune system dysregulation by the way of epigenetic modulation of TET2. These results should be examined in larger, functional studies with diverse population-based cohorts to determine the potential relationships of both SDOH and epigenetic markers in CH and cardio-oncology outcomes. Associations between TET2 methylation sites, SpleenA, SES and Cytokines in DCCNHA cohort, 2014-17 Tet2cg09666717 Tet2cg05094833 Tet2cg10594473 SES 0.310 (0.038) -0.405 (0.006) -0.283 (0.060) Splenic Activity -0.453 (0.036) 0.004 (0.985) 0.097 (0.654) IL-6 -0.078 (0.558) -0.211 (0.108) -0.222 (0.084) IL-8 -0.199 (0.153) 0.024 (0.865) -0.004 (0.979) IL-17A -0.373 (0.010) 0.134 (0.370) -0.434 (0.017) IL-1β -0.382 (0.003) 0.042 (0.757) -0.143 (0.275) TNFα -0.456 (0.000) -0.157 (0.244) 0.005 (0.969) IFN-γ -0.258 (0.062) -0.037 (0.790) 0.022 (0.876) Data are presented as standardized β coefficient (p-value). All data are adjusted for 10-year predicted ASCVD risk and BMI; ASCVD = atherosclerotic cardiovascular disease; BMI = body mass index; IL-6 = interleukin 6; IL-8 = interleukin 8; IL-17A = interleukin 17A; IL-1β = interleukin 1 beta; TNFα = tumor necrosis factor; IFN-γ = interferon gamma Citation Format: Sonal Sharda, Yvonne Baumer, Alina P. Pang, Abhinav Saurabh, Billy S. Collins, Valerie M. Mitchell, Michael J. Corley, Tiffany M. Powell-Wiley. Socioeconomic status associates with epigenetic modulation of TET2: An emerging pathway in cardio-oncology [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 2163.

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Sylvestre, Marvin, Karin Tarte, and David Roulois. "Epigenetic mechanisms driving tumor supportive microenvironment differentiation and function: a role in cancer therapy?" Epigenomics 12, no. 2 (January 2020): 157–69. http://dx.doi.org/10.2217/epi-2019-0165.

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The tumor microenvironment (TME) plays a central role in tumor development and drug resistance. Within TME, the stromal cell subset, called cancer-associated fibroblasts, is a heterogeneous population originating from poorly characterized precursors. Since cancer-associated fibroblasts do not acquire somatic mutations, other mechanisms like epigenetic regulation, could be involved in the development of these cells and in the acquisition of tumor supportive phenotypes. Moreover, such epigenetic modulations have been correlated to the emergence of an immunosuppressive microenvironment facilitating tumor evasion. These findings underline the need to deepen our knowledge on epigenetic mechanisms driving TME development and function, and to understand the impact of epigenetic drugs that could be used in future to target both tumor cells and their TME.

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Tsai, Kun-Ling, Chia-To Wang, Chia-Hua Kuo, Yuan-Yang Cheng, Hsin-I. Ma, Ching-Hsia Hung, Yi-Ju Tsai, and Chung-Lan Kao. "The potential role of epigenetic modulations in BPPV maneuver exercises." Oncotarget 7, no. 24 (May 18, 2016): 35522–34. http://dx.doi.org/10.18632/oncotarget.9446.

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Spencer, Shawal, Agustina Gugliotta, Natascha Gödecke, Hansjörg Hauser, and Dagmar Wirth. "Epigenetic modulations rendering cell-to-cell variability and phenotypic metastability." Journal of Genetics and Genomics 43, no. 8 (August 2016): 503–11. http://dx.doi.org/10.1016/j.jgg.2016.05.008.

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Zhang, Zhenzhen, Changjiu He, Lu Zhang, Tianqi Zhu, Dongying Lv, Guangdong Li, Yukun Song, et al. "Alpha-ketoglutarate affects murine embryo development through metabolic and epigenetic modulations." Reproduction 158, no. 2 (August 2019): 125–35. http://dx.doi.org/10.1530/rep-19-0018.

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α-Ketoglutarate (α-KG) is an intermediary metabolite in the tricarboxylic acid (TCA) cycle and functions to inhibit ATPase and maintain the pluripotency of embryonic stem cells (ESCs); however, little is known regarding the effects of α-KG on the development of preimplantation embryos. Herein, we report that α-KG (150 μM) treatment significantly promoted the blastocyst rate, the number of inner cell mass (ICM) cells and foetal growth after embryo transfer. Mechanistic studies revealed two important pathways involved in the α-KG effects on embryo development. First, α-KG modulates mitochondria function by inducing relatively low ATP production without modification of mitochondrial copy number. The relatively low energy metabolism preserves the pluripotency and competence of the ICM. Second, α-KG modifies epigenetics in embryos cultured in vitro by affecting the activity of the DNA demethylation enzyme TET and the DNA methylation gene Dnmt3a to increase the ratio of 5hmC/5mC ratio. Elevation of the 5hmC/5mC ratio not only promotes the pluripotency of the ICM but also leads to a methylation level in an in vitro embryo close to that in an in vivo embryo. All these functions of α-KG collectively contribute to an increase in the number of ICM cells, leading to greater adaptation of cultured embryos to in vitro conditions and promoting foetal growth after embryo transfer. Our findings provide basic knowledge regarding the mechanisms by which α-KG affects embryo development and cell differentiation.

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Niki Boroujeni, Zahra, Atefeh shirkavand, and Seyed Ahmad Aleyasin. "Epigenetic Modulations Induction Using DSCR1 Ectopic Expression in Breast Cancer Cells." Molecular & Cellular Biomechanics 16, no. 1 (2019): 41–58. http://dx.doi.org/10.32604/mcb.2019.04366.

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Sarkar, Shilpi, Dheepika Venkatesh, Thirukumaran Kandasamy, and Siddhartha Sankar Ghosh. "Epigenetic Modulations in Breast Cancer: An Emerging Paradigm in Therapeutic Implications." Frontiers in Bioscience-Landmark 29, no. 8 (August 19, 2024): 287. http://dx.doi.org/10.31083/j.fbl2908287.

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Xu, Yuanchun, Zongsheng He, Jing Du, Ziqiang Chen, John W. M. Creemers, Bin Wang, Fan Li, and Yaling Wang. "Epigenetic modulations of immune cells: from normal development to tumor progression." International Journal of Biological Sciences 19, no. 16 (2023): 5120–44. http://dx.doi.org/10.7150/ijbs.88327.

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Jasek, Karin, Peter Kubatka, Marek Samec, Alena Liskova, Karel Smejkal, Desanka Vybohova, Ondrej Bugos, et al. "DNA Methylation Status in Cancer Disease: Modulations by Plant-Derived Natural Compounds and Dietary Interventions." Biomolecules 9, no. 7 (July 18, 2019): 289. http://dx.doi.org/10.3390/biom9070289.

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The modulation of the activity of DNA methyltransferases (DNMTs) represents a crucial epigenetic mechanism affecting gene expressions or DNA repair mechanisms in the cells. Aberrant modifications in the function of DNMTs are a fundamental event and part of the pathogenesis of human cancer. Phytochemicals, which are biosynthesized in plants in the form of secondary metabolites, represent an important source of biomolecules with pleiotropic effects and thus provide a wide range of possible clinical applications. It is well documented that phytochemicals demonstrate significant anticancer properties, and in this regard, rapid development within preclinical research is encouraging. Phytochemicals affect several epigenetic molecular mechanisms, including DNA methylation patterns such as the hypermethylation of tumor-suppressor genes and the global hypomethylation of oncogenes, that are specific cellular signs of cancer development and progression. This review will focus on the latest achievements in using plant-derived compounds and plant-based diets targeting epigenetic regulators and modulators of gene transcription in preclinical and clinical research in order to generate novel anticancer drugs as sensitizers for conventional therapy or compounds suitable for the chemoprevention clinical setting in at-risk individuals. In conclusion, indisputable anticancer activities of dietary phytochemicals linked with proper regulation of DNA methylation status have been described. However, precisely designed and well-controlled clinical studies are needed to confirm their beneficial epigenetic effects after long-term consumption in humans.

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Bastida, Guillermo, Alejandro Mínguez, Pilar Nos, and Inés Moret-Tatay. "Immunoepigenetic Regulation of Inflammatory Bowel Disease: Current Insights into Novel Epigenetic Modulations of the Systemic Immune Response." Genes 14, no. 3 (February 23, 2023): 554. http://dx.doi.org/10.3390/genes14030554.

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The immune system and environmental factors are involved in various diseases, such as inflammatory bowel disease (IBD), through their effect on genetics, which modulates immune cells. IBD encompasses two main phenotypes, Crohn’s disease, and ulcerative colitis, which are manifested as chronic and systemic relapse-remitting gastrointestinal tract disorders with rising global incidence and prevalence. The pathophysiology of IBD is complex and not fully understood. Epigenetic research has resulted in valuable information for unraveling the etiology of this immune-mediated disease. Thus, the main objective of the present review is to summarize the current findings on the role of epigenetic mechanisms in IBD to shed light on their potential clinical relevance. This review focuses on the latest evidence regarding peripheral blood mononuclear cells and epigenetic changes in histone modification, DNA methylation, and telomere shortening in IBD. The various identified epigenetic DNA profiles with clinical value in IBD could be used as biomarkers for more accurately predicting disease development, treatment response, and therapy-related adverse events. Ultimately, the information presented here could be of potential relevance for future clinical practice in developing more efficient and precise medicine to improve the quality of life for patients with IBD.

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Fan, Chaofan, Shing Kam, and Pierluigi Ramadori. "Metabolism-Associated Epigenetic and Immunoepigenetic Reprogramming in Liver Cancer." Cancers 13, no. 20 (October 19, 2021): 5250. http://dx.doi.org/10.3390/cancers13205250.

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Metabolic reprogramming and epigenetic changes have been characterized as hallmarks of liver cancer. Independently of etiology, oncogenic pathways as well as the availability of different energetic substrates critically influence cellular metabolism, and the resulting perturbations often cause aberrant epigenetic alterations, not only in cancer cells but also in the hepatic tumor microenvironment. Metabolic intermediates serve as crucial substrates for various epigenetic modulations, from post-translational modification of histones to DNA methylation. In turn, epigenetic changes can alter the expression of metabolic genes supporting on the one hand, the increased energetic demand of cancer cells and, on the other hand, influence the activity of tumor-associated immune cell populations. In this review, we will illustrate the most recent findings about metabolic reprogramming in liver cancer. We will focus on the metabolic changes characterizing the tumor microenvironment and on how these alterations impact on epigenetic mechanisms involved in the malignant progression. Furthermore, we will report our current knowledge about the influence of cancer-specific metabolites on epigenetic reprogramming of immune cells and we will highlight how this favors a tumor-permissive immune environment. Finally, we will review the current strategies to target metabolic and epigenetic pathways and their therapeutic potential in liver cancer, alone or in combinatorial approaches.

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Yi, Sang Ah, Ki Hong Nam, Min Gyu Lee, Hwamok Oh, Jae Sung Noh, Jae Kyun Jeong, Sangwoo Kwak, et al. "Transcriptomics-Based Repositioning of Natural Compound, Eudesmin, as a PRC2 Modulator." Molecules 26, no. 18 (September 18, 2021): 5665. http://dx.doi.org/10.3390/molecules26185665.

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Extensive epigenetic remodeling occurs during the cell fate determination of stem cells. Previously, we discovered that eudesmin regulates lineage commitment of mesenchymal stem cells through the inhibition of signaling molecules. However, the epigenetic modulations upon eudesmin treatment in genomewide level have not been analyzed. Here, we present a transcriptome profiling data showing the enrichment in PRC2 target genes by eudesmin treatment. Furthermore, gene ontology analysis showed that PRC2 target genes downregulated by eudesmin are closely related to Wnt signaling and pluripotency. We selected DKK1 as an eudesmin-dependent potential top hub gene in the Wnt signaling and pluripotency. Through the ChIP-qPCR and RT-qPCR, we found that eudesmin treatment increased the occupancy of PRC2 components, EZH2 and SUZ12, and H3K27me3 level on the promoter region of DKK1, downregulating its transcription level. According to the analysis of GEO profiles, DEGs by depletion of Oct4 showed an opposite pattern to DEGs by eudesmin treatment. Indeed, the expression of pluripotency markers, Oct4, Sox2, and Nanog, was upregulated upon eudesmin treatment. This finding demonstrates that pharmacological modulation of PRC2 dynamics by eudesmin might control Wnt signaling and maintain pluripotency of stem cells.

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Soldado-Gordillo, Alba, and Ana Isabel Álvarez-Mercado. "Epigenetics, Microbiota, and Breast Cancer: A Systematic Review." Life 14, no. 6 (May 30, 2024): 705. http://dx.doi.org/10.3390/life14060705.

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Breast cancer is the most frequently diagnosed cancer in women worldwide. According to recent studies, alterations in the microbiota and epigenetic modulations are risk factors for this disease. This systematic review aims to determine the possible associations between the intestinal and mammary microbial populations, epigenetic modifications, and breast cancer. To achieve this objective, we conducted a literature search in the PubMed, Web of Science, and Science Direct databases following the PRISMA guidelines. Although no results are yet available in humans, studies in mice suggest a protective effect of maternal dietary interventions with bioactive compounds on the development of breast tumors in offspring. These dietary interventions also modified the gut microbiota, increasing the relative abundance of short-chain fatty acid-producing taxa and preventing mammary carcinogenesis. In addition, short-chain fatty acids produced by the microbiota act as epigenetic modulators. Furthermore, some authors indicate that stress alters the gut microbiota, promoting breast tumor growth through epigenetic and gene expression changes in the breast tumor microenvironment. Taken together, these findings show the ability of epigenetic modifications and alterations of the microbiota associated with environmental factors to modulate the development, aggressiveness, and progression of breast cancer.

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Wang, Shanzheng, Anne Jenseit, Jens-Martin Hübner, Monika Mauermann, Konstantin Okonechnikov, Stefan M. Pfister, and Marcel Kool. "EPEN-11. CHARACTERIZING EPIGENETIC MODULATIONS AND EZHIP DOWNSTREAM TARGETS IN PFA EPENDYMOMA." Neuro-Oncology 26, Supplement_4 (June 18, 2024): 0. http://dx.doi.org/10.1093/neuonc/noae064.213.

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Abstract BACKGROUND Ependymomas can arise from all compartments of the central nervous system and ten distinct molecular groups have been identified in children and adults. In children, the most aggressive group is posterior fossa group A ependymoma (PFA). In PFA ependymomas, the aberrant overexpression of EZHIP (EZH inhibitory protein) has been implicated as a relevant driver of the disease. EZHIP suppresses the installing and spreading of the repressive epigenetic mark H3K27me3 via disturbing PRC2 (polycomb repressive complex 2) activity through inhibiting EZH2 (enhancer of zeste 2), which causes overall low levels of H3K27me3 in PFA. METHODS To get a better understanding how EZHIP may drive the disease, how it affects the epigenetic landscape and what the downstream targets of EZHIP are, we performed DNA sequencing, RNA expression profiling and ChIP-seq experiments of H3K27me3, H3K27ac, EZH2, and EZHIP in PFA, PFB, and ST-ZFTA ependymomas (n = 3 tumor cases each). RESULTS After validating the high levels of EZHIP and global reduction of H3K27me3 in PFA, we characterized the epigenetic landscape and EZHIP chromatin binding characteristics in PFA compared to PFB and ST-ZFTA ependymoma. Transcriptome analysis showed that overall more genes are up-regulated in PFA compared with PFB and ZFTA, which might be caused by its relatively high accessibility with a global loss of H3K27me3. EZHIP knockdown experiments confirmed direct changes on H3K27me3, H3K27ac and gene expression. We also found that PLAG1 (pleomorphic adenoma gene 1) expression linearly correlated with EZHIP expression in PFA tumors. ChIP-seq data indeed showed the PLAG1 locus to be bound by EZHIP and marked with increased H3K27ac and decreased H3K27me3 signals in PFA. CONCLUSIONS We identified PLAG1 as a potential downstream target of EZHIP in PFA tumors. Currently, more experiments on PLAG1 are being performed to further explore its role as a potential vulnerability in PFA ependymoma.

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Shirkavand, Atefeh, Zahra N. Boroujeni, and Seyed A. Aleyasin. "Solanum nigrum Anticancer Effect Through Epigenetic Modulations in Breast Cancer Cell Lines." Current Cancer Therapy Reviews 16, no. 2 (June 9, 2020): 121–26. http://dx.doi.org/10.2174/1573394715666190101114541.

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Background: DNA methylation plays an important role in the regulation of gene expression in mammalian cells and often occurs at CpG islands in the genome. It is more reversible than genetic variations and has therefore attracted much attention for the treatment of many diseases, especially cancer. In the present study, we investigated the effect of Solanum nigrum Extract (SNE) on the methylation status of the VIM and CXCR4 genes in breast cancer cell lines. Methods: The Trypan blue assay was used to study the effect of SNE at various concentrations of 0, 0.1, 1.5, 2.5, 3.5 and 5 mg/ml for 48 h on the survival of three human breast cancer cell lines MCF7, MDA-MB-468, MDA-MB-231. Methylation status of VIM and CXCR4 genes in breast cancer cell lines was assessed by Methylation-Specific PCR (MSP) method. Also, methylation changes of VIM and CXCR4 genes in breast cancer cell lines after treatment with 0.1 mg/ml of SNE for 6 days were analyzed by MSP method. To confirm the effect of SNE on methylation of VIM and CXCR4 genes, Real-Time PCR was performed. Results: The Trypan blue assay results indicated that treatment with SNE reduced cell viability in a dose-dependent manner in breast cancer cells. Our results showed that treatment of breast cancer cells with 0.1 mg/ml of SNE hypermethylated the VIM, CXCR4 genes and significantly reduced the expression levels of their mRNA (P<0.05). Conclusion: Our findings reveal for the first time the impact of SNE on the methylation of breast cancer cells.

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Huang, Chengyang, and Joseph C. Wu. "Epigenetic modulations of induced pluripotent stem cells: novel therapies and disease models." Drug Discovery Today: Disease Models 9, no. 4 (December 2012): e153-e160. http://dx.doi.org/10.1016/j.ddmod.2012.02.004.

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Ghasemi, Hatef, Maryam Nazm Bojnordi, and Hossein Azizi. "Epigenetic modulations of neurogenic differentiation of human bone marrow-derived mesenchymal cells." Experimental Hematology 44, no. 9 (September 2016): S108. http://dx.doi.org/10.1016/j.exphem.2016.06.242.

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Wajda, Anna, Joanna Łapczuk-Romańska, and Agnieszka Paradowska-Gorycka. "Epigenetic Regulations of AhR in the Aspect of Immunomodulation." International Journal of Molecular Sciences 21, no. 17 (September 3, 2020): 6404. http://dx.doi.org/10.3390/ijms21176404.

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Environmental factors contribute to autoimmune disease manifestation, and as regarded today, AhR has become an important factor in studies of immunomodulation. Besides immunological aspects, AhR also plays a role in pharmacological, toxicological and many other physiological processes such as adaptive metabolism. In recent years, epigenetic mechanisms have provided new insight into gene regulation and reveal a new contribution to autoimmune disease pathogenesis. DNA methylation, histone modifications, chromatin alterations, microRNA and consequently non-genetic changes in phenotypes connect with environmental factors. Increasing data reveals AhR cross-roads with the most significant in immunology pathways. Although study on epigenetic modulations in autoimmune diseases is still not well understood, therefore future research will help us understand their pathophysiology and help to find new therapeutic strategies. Present literature review sheds the light on the common ground between remodeling chromatin compounds and autoimmune antibodies used in diagnostics. In the proposed review we summarize recent findings that describe epigenetic factors which regulate AhR activity and impact diverse immunological responses and pathological changes.

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Li, Song. "Benefits of physical exercise on Alzheimer's disease: an epigenetic view." Ageing and Neurodegenerative Diseases 3, no. 2 (2023): 6. http://dx.doi.org/10.20517/and.2022.37.

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Increasing lines of evidence have indicated the beneficial impacts of exercise on the neurodegeneration and cognitive decline of Alzheimer’s disease (AD). While general mechanisms underlying the positive effects, including the elevated neurotrophins level, improved neurogenesis and neuroplasticity, restored angiogenesis and autophagy, and reduced neuroinflammation, have been well documented, the epigenetic mechanisms of exercise on AD, however, are still inconclusive. Exercise can regulate the expression of those AD-related genes or proteins through various epigenetic modulations, thereafter rescuing AD pathologies and improving cognitive deficits of AD. In this review, we briefly summarized recent research advances in the beneficial impacts of exercise on cognition and AD and discussed the underlying mechanisms from an epigenetic point of view, including DNA methylation, histone modifications, and non-coding RNAs. A deep understanding of how exercise epigenetically promotes cognitive and pathological recoveries in AD is crucial for the future discovery of precise exercise procedures or exercise-like remedies to treat this disease.

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Kumar, Suresh, Karishma Seem, and Trilochan Mohapatra. "Biochemical and Epigenetic Modulations under Drought: Remembering the Stress Tolerance Mechanism in Rice." Life 13, no. 5 (May 10, 2023): 1156. http://dx.doi.org/10.3390/life13051156.

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A plant, being a sessile organism, needs to modulate biochemical, physiological, and molecular responses to the environment in a quick and efficient manner to be protected. Drought stress is a frequently occurring abiotic stress that severely affects plant growth, development, and productivity. Short- and long-term memories are well-known phenomena in animals; however, the existence of such remembrance in plants is still being discovered. In this investigation, different rice genotypes were imposed with drought stress just before flowering and the plants were re-watered for recovery from the stress. Seeds collected from the stress-treated (stress-primed) plants were used to raise plants for the subsequent two generations under a similar experimental setup. Modulations in physio-biochemical (chlorophyll, total phenolics and proline contents, antioxidant potential, lipid peroxidation) and epigenetic [5-methylcytosine (5-mC)] parameters were analyzed in the leaves of the plants grown under stress as well as after recovery. There was an increase in proline (>25%) and total phenolic (>19%) contents, antioxidant activity (>7%), and genome-wide 5-mC level (>56%), while a decrease (>9%) in chlorophyll content was recorded to be significant under the stress. Interestingly, a part of the increased proline content, total phenolics content, antioxidant activity, and 5-mC level was retained even after the withdrawal of the stress. Moreover, the increased levels of biochemical and epigenetic parameters were observed to be transmitted/inherited to the subsequent generations. These might help in developing stress-tolerant crops and improving crop productivity under the changing global climate for sustainable food production and global food security.

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Jia, Xiao, Jiayi Song, Yijian Wu, Sai Feng, Zeao Sun, Yan Hu, Mengxue Yu, Rui Han, and Bin Zeng. "Strategies for the Enhancement of Secondary Metabolite Production via Biosynthesis Gene Cluster Regulation in Aspergillus oryzae." Journal of Fungi 10, no. 5 (April 25, 2024): 312. http://dx.doi.org/10.3390/jof10050312.

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The filamentous fungus Aspergillus oryzae (A. oryzae) has been extensively used for the biosynthesis of numerous secondary metabolites with significant applications in agriculture and food and medical industries, among others. However, the identification and functional prediction of metabolites through genome mining in A. oryzae are hindered by the complex regulatory mechanisms of secondary metabolite biosynthesis and the inactivity of most of the biosynthetic gene clusters involved. The global regulatory factors, pathway-specific regulatory factors, epigenetics, and environmental signals significantly impact the production of secondary metabolites, indicating that appropriate gene-level modulations are expected to promote the biosynthesis of secondary metabolites in A. oryzae. This review mainly focuses on illuminating the molecular regulatory mechanisms for the activation of potentially unexpressed pathways, possibly revealing the effects of transcriptional, epigenetic, and environmental signal regulation. By gaining a comprehensive understanding of the regulatory mechanisms of secondary metabolite biosynthesis, strategies can be developed to enhance the production and utilization of these metabolites, and potential functions can be fully exploited.

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Breuls, Natacha, Giorgia Giacomazzi, and Maurilio Sampaolesi. "(Epi)genetic Modifications in Myogenic Stem Cells: From Novel Insights to Therapeutic Perspectives." Cells 8, no. 5 (May 9, 2019): 429. http://dx.doi.org/10.3390/cells8050429.

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The skeletal muscle is considered to be an ideal target for stem cell therapy as it has an inherent regenerative capacity. Upon injury, the satellite cells, muscle stem cells that reside under the basal lamina of the myofibres, start to differentiate in order to reconstitute the myofibres while maintaining the initial stem cell pool. In recent years, it has become more and more evident that epigenetic mechanisms such as histon modifications, DNA methylations and microRNA modulations play a pivatol role in this differentiation process. By understanding the mechanisms behind myogenesis, researchers are able to use this knowledge to enhance the differentiation and engraftment potential of different muscle stem cells. Besides manipulation on an epigenetic level, recent advances in the field of genome-engineering allow site-specific modifications in the genome of these stem cells. Combining epigenetic control of the stem cell fate with the ability to site-specifically correct mutations or add genes for further cell control, can increase the use of stem cells as treatment of muscular dystrophies drastically. In this review, we will discuss the advances that have been made in genome-engineering and the epigenetic regulation of muscle stem cells and how this knowledge can help to get stem cell therapy to its full potential.

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Vilpoux, C., I. Drissi, P. Gosset, C. Roger, J. Chagas Ricardo, A. Robert, M. Naassila, and O. Pierrefiche. "Two binges of ethanol a day induces epigenetic modulations and astrogliosis in adolescent rats." European Neuropsychopharmacology 27 (October 2017): S1049. http://dx.doi.org/10.1016/s0924-977x(17)31832-1.

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Su, Yueqing, Xuemei Liu, Jiamei Lian, and Chao Deng. "Epigenetic histone modulations of PPARγ and related pathways contribute to olanzapine-induced metabolic disorders." Pharmacological Research 155 (May 2020): 104703. http://dx.doi.org/10.1016/j.phrs.2020.104703.

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Borutinskaitė, Veronika, Aida Virkšaitė, Giedrė Gudelytė, and Rūta Navakauskienė. "Green tea polyphenol EGCG causes anti-cancerous epigenetic modulations in acute promyelocytic leukemia cells." Leukemia & Lymphoma 59, no. 2 (June 22, 2017): 469–78. http://dx.doi.org/10.1080/10428194.2017.1339881.

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Cavaleiro, Carla Sofia. "DBS- induced epigenetic modulations over memory deficits in MeCP2-related disorders: a literature review." Brain Stimulation 16, no. 1 (January 2023): 259. http://dx.doi.org/10.1016/j.brs.2023.01.425.

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Siomek-Gorecka, Agnieszka, Anna Dlugosz, and Damian Czarnecki. "The Molecular Basis of Alcohol Use Disorder (AUD). Genetics, Epigenetics, and Nutrition in AUD: An Amazing Triangle." International Journal of Molecular Sciences 22, no. 8 (April 20, 2021): 4262. http://dx.doi.org/10.3390/ijms22084262.

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Alcohol use disorder (AUD) is a very common and complex disease, as alcohol is the most widely used addictive drug in the world. This disorder has an enormous impact on public health and social and private life, and it generates a huge number of social costs. Alcohol use stimulates hypothalamic–pituitary–adrenal (HPA) axis responses and is the cause of many physical and social problems (especially liver disease and cancer), accidental injury, and risky sexual behavior. For years, researchers have been trying to identify the genetic basis of alcohol use disorder, the molecular mechanisms responsible for its development, and an effective form of therapy. Genetic and environmental factors are known to contribute to the development of AUD, and the expression of genes is a complicated process that depends on epigenetic modulations. Dietary nutrients, such as vitamins, may serve as one these modulators, as they have a direct impact on epigenomes. In this review, we connect gathered knowledge from three emerging fields—genetics, epigenetics, and nutrition—to form an amazing triangle relating to alcohol use disorder.

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Tung, Shu-Yun, Sue-Hong Wang, Sue-Ping Lee, Shu-Ping Tsai, Hsiao-Hsuian Shen, Feng-Jung Chen, Yu-Yi Wu, Sheng-Pin Hsiao, and Gunn-Guang Liou. "Modulations of SIR-nucleosome interactions of reconstructed yeast silent pre-heterochromatin by O-acetyl-ADP-ribose and magnesium." Molecular Biology of the Cell 28, no. 3 (February 2017): 381–86. http://dx.doi.org/10.1091/mbc.e16-06-0359.

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Yeast silent heterochromatin provides an excellent model with which to study epigenetic inheritance. Previously we developed an in vitro assembly system to demonstrate the formation of filament structures with requirements that mirror yeast epigenetic gene silencing in vivo. However, the properties of these filaments were not investigated in detail. Here we show that the assembly system requires Sir2, Sir3, Sir4, nucleosomes, and O-acetyl-ADP-ribose. We also demonstrate that all Sir proteins and nucleosomes are components of these filaments to prove that they are SIR-nucleosome filaments. Furthermore, we show that the individual localization patterns of Sir proteins on the SIR-nucleosome filament reflect those patterns on telomeres in vivo. In addition, we reveal that magnesium exists in the SIR-nucleosome filament, with a role similar to that for chromatin condensation. These results suggest that a small number of proteins and molecules are sufficient to mediate the formation of a minimal yeast silent pre-heterochromatin in vitro.

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Tseng, Yen-Tzu, Hung-Fu Liao, Chih-Yun Yu, Chu-Fan Mo, and Shau-Ping Lin. "Epigenetic factors in the regulation of prospermatogonia and spermatogonial stem cells." REPRODUCTION 150, no. 3 (September 2015): R77—R91. http://dx.doi.org/10.1530/rep-14-0679.

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Appropriate regulation of epigenome within cells is crucial for the determination of cell fate and contributes to the lifelong maintenance of tissue homeostasis. Epigenomic re-establishment during embryonic prospermatogonia development and fine-tune of the epigenetic landscape in postnatal spermatogonial stem cells (SSCs) are two key processes required for functional male germ cell formation. Repression of re-activated transposons and male germline-specific epigenome establishment occur in prospermatogonia, whereas modulations of the epigenetic landscape is important for SSC self-renewal and differentiation to maintain the stem cell pool and support long-term sperm production. Here, we describe the impact of epigenome-related regulators and small non-coding RNAs as well as the influence of epigenome modifications that result from extrinsic signaling for controlling the decision between self-renewal, differentiation and survival in mouse prospermatogonia and SSCs. This article provides a review of epigenome-related molecules involved in cell fate determination in male germ cells and discusses the intriguing questions that arise from these studies.

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Veronesi, Francesca, Viviana Costa, Daniele Bellavia, Valentina Basoli, and Gianluca Giavaresi. "Epigenetic Modifications of MiRNAs in Osteoarthritis: A Systematic Review on Their Methylation Levels and Effects on Chondrocytes, Extracellular Matrix and Joint Inflammation." Cells 12, no. 14 (July 11, 2023): 1821. http://dx.doi.org/10.3390/cells12141821.

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Osteoarthritis (OA) is a joint disorder characterized by progressive degeneration of cartilage extracellular matrix (ECM), chondrocyte hypertrophy and apoptosis and inflammation. The current treatments mainly concern pain control and reduction of inflammation, but no therapeutic strategy has been identified as a disease-modifying treatment. Therefore, identifying specific biomarkers useful to prevent, treat or distinguish the stages of OA disease has become an immediate need of clinical practice. The role of microRNAs (miRNAs) in OA has been investigated in the last decade, and increasing evidence has emerged that the influence of the environment on gene expression through epigenetic processes contributes to the development, progression and aggressiveness of OA, in particular acting on the microenvironment modulations. The effects of epigenetic regulation, particularly different miRNA methylation during OA disease, were highlighted in the present systematic review. The evidence arising from this study of the literature conducted in three databases (PubMed, Scopus, Web of Science) suggested that miRNA methylation state already strongly impacts OA progression, driving chondrocytes and synoviocyte proliferation, apoptosis, inflammation and ECM deposition. However, the possibility of understanding the mechanism by which different epigenetic modifications of miRNA or pre-miRNA sequences drive the aggressiveness of OA could be the new focus of future investigations.

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Fernandes, Valencia, Dharmendra Khatri, and Shashi Singh. "Lipototxiciy alters the chaperones and synaptic fidelity via epigenetic modulations in mammalian derived hippocampal cells." Journal of the Neurological Sciences 429 (October 2021): 118279. http://dx.doi.org/10.1016/j.jns.2021.118279.

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Maricato, Juliana T., Maria N. Furtado, Maisa C. Takenaka, Edsel R. M. Nunes, Patricia Fincatti, Fabiana M. Meliso, Ismael D. C. G. da Silva, et al. "Epigenetic Modulations in Activated Cells Early after HIV-1 Infection and Their Possible Functional Consequences." PLOS ONE 10, no. 4 (April 13, 2015): e0119234. http://dx.doi.org/10.1371/journal.pone.0119234.

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Hayashi, Kaori. "Editorial (Thematic Issue: Epigenetic Modulations in Kidney Podocytes: A Possible Target of Treatment for Proteinuria)." Current Hypertension Reviews 12, no. 2 (May 24, 2016): 88. http://dx.doi.org/10.2174/157340211202160525001108.

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Choate, Kristian A., Evan P. S. Pratt, Matthew J. Jennings, Robert J. Winn, and Paul B. Mann. "IDH Mutations in Glioma: Molecular, Cellular, Diagnostic, and Clinical Implications." Biology 13, no. 11 (October 30, 2024): 885. http://dx.doi.org/10.3390/biology13110885.

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In 2021, the World Health Organization classified isocitrate dehydrogenase (IDH) mutant gliomas as a distinct subgroup of tumors with genetic changes sufficient to enable a complete diagnosis. Patients with an IDH mutant glioma have improved survival which has been further enhanced by the advent of targeted therapies. IDH enzymes contribute to cellular metabolism, and mutations to specific catalytic residues result in the neomorphic production of D-2-hydroxyglutarate (D-2-HG). The accumulation of D-2-HG results in epigenetic alterations, oncogenesis and impacts the tumor microenvironment via immunological modulations. Here, we summarize the molecular, cellular, and clinical implications of IDH mutations in gliomas as well as current diagnostic techniques.

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Journal articles on the topic 'Epigenetic Modulations'

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