scholarly journals Epigenetic Regulation of microRNAs in Cancer: Shortening the Distance from Bench to Bedside

2021 ◽  
Vol 22 (14) ◽  
pp. 7350
Author(s):  
María J. Pajares ◽  
Ester Alemany-Cosme ◽  
Saioa Goñi ◽  
Eva Bandres ◽  
Cora Palanca-Ballester ◽  
...  
Keyword(s):  
Complex Disease ◽  
Epigenetic Factors ◽  
Clinical Value ◽  
Cellular Processes ◽  
Cancer Management ◽  
Promising Strategy ◽  
Epigenetic Machinery ◽  
Multiple Processes ◽  
Relevant Role ◽  
Non Coding Rnas

Cancer is a complex disease involving alterations of multiple processes, with both genetic and epigenetic features contributing as core factors to the disease. In recent years, it has become evident that non-coding RNAs (ncRNAs), an epigenetic factor, play a key role in the initiation and progression of cancer. MicroRNAs, the most studied non-coding RNAs subtype, are key controllers in a myriad of cellular processes, including proliferation, differentiation, and apoptosis. Furthermore, the expression of miRNAs is controlled, concomitantly, by other epigenetic factors, such as DNA methylation and histone modifications, resulting in aberrant patterns of expression upon the occurrence of cancer. In this sense, aberrant miRNA landscape evaluation has emerged as a promising strategy for cancer management. In this review, we have focused on the regulation (biogenesis, processing, and dysregulation) of miRNAs and their role as modulators of the epigenetic machinery. We have also highlighted their potential clinical value, such as validated diagnostic and prognostic biomarkers, and their relevant role as chromatin modifiers in cancer therapy.

scholarly journals Overview on Epigenetics and Cancer

2020 ◽  
Vol 2 (3) ◽  
pp. 01-06
Author(s):  
Eman Youness
Keyword(s):  
Metabolic Diseases ◽  
Chemical Processes ◽  
Epigenetic Alterations ◽  
Epigenetic Factors ◽  
Cancer Epigenetics ◽  
Expression Studies ◽  
Epigenetic Machinery ◽  
Non Coding Rnas ◽  
New Strategies ◽  
Genotype A

Epigenetics is considered as the science of hereditary phenotype which does not encompass amendment in the DNA. This occurs through chemical processes that modify the phenotype, without altering the genotype. A large number of studies showed that metabolic diseases are highly associated with epigenetic alterations suggesting that epigenetic factors may play a central role in cancer. Recent advancements in the rapidly evolving field of cancer epigenetics have shown extensive reprogramming of every component of the epigenetic machinery in cancer including DNA methylation, histone modifications, nucleosome positioning and non-coding RNAs, specifically microRNA expression. Studies of the mechanism(s) of epigenetic regulation and its reversibility have resulted in the identification of novel targets that may be useful in developing new strategies for the prevention and treatment of cancer.

scholarly journals Interplay between long non-coding RNAs and epigenetic machinery: emerging targets in cancer?

2018 ◽  
Vol 373 (1748) ◽  
pp. 20170074 ◽  
Author(s):  
David J. Hanly ◽  
Manel Esteller ◽  
María Berdasco
Keyword(s):  
Nuclear Architecture ◽  
Epigenetic Factors ◽  
Histone Methyltransferases ◽  
Epigenetic Modifiers ◽  
Protein Partners ◽  
Epigenetic Machinery ◽  
Human Disorders ◽  
Transcription Modulation ◽  
Non Coding Rnas ◽  
Epigenetic Research

Of the diverse array of putative molecular and biological functions assigned to long non-coding RNAs (lncRNAs), one attractive perspective in epigenetic research has been the hypothesis that lncRNAs directly interact with the proteins involved in the modulation of chromatin conformation. Indeed, epigenetic modifiers are among the most frequent protein partners of lncRNAs that have been identified to date, of which histone methyltransferases and protein members of the Polycomb Repressive Complex PRC2 have received considerable attention. This review is focused on how lncRNAs interface with epigenetic factors to shape the outcomes of crucial biological processes such as regulation of gene transcription, modulation of nuclear architecture, X inactivation in females and pre-mRNA splicing. Because of our increasing knowledge of their role in development and cellular differentiation, more research is beginning to be done into the deregulation of lncRNAs in human disorders. Focusing on cancer, we describe some key examples of disease-focused lncRNA studies. This knowledge has significantly contributed to our ever-improving understanding of how lncRNAs interact with epigenetic factors of human disease, and has also provided a plethora of much-needed novel prognostic biomarker candidates or potential therapeutic targets. Finally, current limitations and perspectives on lncRNA research are discussed here. This article is part of a discussion meeting issue ‘Frontiers in epigenetic chemical biology’.

scholarly journals Interaction among inflammasome, autophagy and non-coding RNAs: new horizons for drug

2019 ◽  
Vol 2 (3) ◽  
pp. 166-182 ◽  
Author(s):  
Qinqin Pu ◽  
Ping Lin ◽  
Zhihan Wang ◽  
Pan Gao ◽  
Shugang Qin ◽  
...  
Keyword(s):  
Drug Targets ◽  
Metabolic Diseases ◽  
Immune Defense ◽  
Inflammasome Activation ◽  
New Horizons ◽  
Cellular Processes ◽  
Multiple Processes ◽  
Non Coding Rnas ◽  
Clinical Conditions ◽  
Refractory Diseases

Abstract Autophagy and inflammasomes are shown to interact in various situations including infectious disease, cancer, diabetes and neurodegeneration. Since multiple layers of molecular regulators contribute to the interplay between autophagy and inflammasome activation, the detail of such interplay remains largely unknown. Non-coding RNAs (ncRNAs), which have been implicated in regulating an expanding list of cellular processes including immune defense against pathogens and inflammatory response in cancer and metabolic diseases, may join in the crosstalk between inflammasomes and autophagy in physiological or disease conditions. In this review, we summarize the latest research on the interlink among ncRNAs, inflammasomes and autophagy and discuss the emerging role of these three in multiple signaling transduction pathways involved in clinical conditions. By analyzing these intriguing interconnections, we hope to unveil the mechanism inter-regulating these multiple processes and ultimately discover potential drug targets for some refractory diseases.

scholarly journals Metastasis is altered through multiple processes regulated by the E2F1 transcription factor

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Matthew R. Swiatnicki ◽  
Eran R. Andrechek
Keyword(s):  
Breast Cancer ◽  
Transgenic Mouse Models ◽  
Cellular Processes ◽  
Mouse Tumors ◽  
Mutation Burden ◽  
Multiple Processes ◽  
Metastatic Process ◽  
Cycle Regulation ◽  
Bioinformatic Approach ◽  
Complicated Nature

AbstractThe E2F family of transcription factors is important for many cellular processes, from their canonical role in cell cycle regulation to other roles in angiogenesis and metastasis. Alteration of the Rb/E2F pathway occurs in various forms of cancer, including breast cancer. E2F1 ablation has been shown to decrease metastasis in MMTV-Neu and MMTV-PyMT transgenic mouse models of breast cancer. Here we take a bioinformatic approach to determine the E2F1 regulated genomic alterations involved in the metastatic cascade, in both Neu and PyMT models. Through gene expression analysis, we reveal few transcriptome changes in non-metastatic E2F1−/− tumors relative to transgenic tumor controls. However investigation of these models through whole genome sequencing found numerous differences between the models, including differences in the proposed tumor etiology between E2F1−/− and E2F1+/+ tumors induced by Neu or PyMT. For example, loss of E2F1 within the Neu model led to an increased contribution of the inefficient double stranded break repair signature to the proposed etiology of the tumors. While the SNV mutation burden was higher in PyMT mouse tumors than Neu mouse tumors, there was no statistically significant differences between E2F WT and E2F1 KO mice. Investigating mutated genes through gene set analysis also found a significant number of genes mutated in the cell adhesion pathway in E2F1−/− tumors, indicating this may be a route for disruption of metastasis in E2F1−/− tumors. Overall, these findings illustrate the complicated nature of uncovering drivers of the metastatic process.

scholarly journals MicroRNA expression profile in bovine mammary gland parenchyma infected by coagulase-positive or coagulase-negative staphylococci

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Emilia Bagnicka ◽  
Ewelina Kawecka-Grochocka ◽  
Klaudia Pawlina-Tyszko ◽  
Magdalena Zalewska ◽  
Aleksandra Kapusta ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Immune System ◽  
Differentially Expressed ◽  
Bacterial Invasion ◽  
Coagulase Negative Staphylococci ◽  
Cellular Processes ◽  
Differentially Expressed Mirnas ◽  
Non Coding Rnas ◽  
Coagulase Positive Staphylococci ◽  
Generation Sequencing

AbstractMicroRNAs (miRNAs) are short, non-coding RNAs, 21–23 nucleotides in length which are known to regulate biological processes that greatly impact immune system activity. The aim of the study was to compare the miRNA expression in non-infected (H) mammary gland parenchyma samples with that of glands infected with coagulase-positive staphylococci (CoPS) or coagulase-negative staphylococci (CoNS) using next-generation sequencing. The miRNA profile of the parenchyma was found to change during mastitis, with its profile depending on the type of pathogen. Comparing the CoPS and H groups, 256 known and 260 potentially new miRNAs were identified, including 32 that were differentially expressed (p ≤ 0.05), of which 27 were upregulated and 5 downregulated. Comparing the CoNS and H groups, 242 known and 171 new unique miRNAs were identified: 10 were upregulated (p ≤ 0.05), and 2 downregulated (p ≤ 0.05). In addition, comparing CoPS with H and CoNS with H, 5 Kyoto Encyclopedia of Genes and Genomes pathways were identified; in both comparisons, differentially-expressed miRNAs were associated with the bacterial invasion of epithelial cells and focal adhesion pathways. Four gene ontology terms were identified in each comparison, with 2 being common to both immune system processes and signal transduction. Our results indicate that miRNAs, especially miR-99 and miR-182, play an essential role in the epigenetic regulation of a range of cellular processes, including immunological systems bacterial growth in dendritic cells and disease pathogenesis (miR-99), DNA repair and tumor progression (miR-182).

scholarly journals Considerations when investigating lncRNA function in vivo

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Andrew R Bassett ◽  
Asifa Akhtar ◽  
Denise P Barlow ◽  
Adrian P Bird ◽  
Neil Brockdorff ◽  
...  
Keyword(s):  
Normal Cell ◽  
Regulatory Elements ◽  
Genomic Locus ◽  
Cellular Processes ◽  
Cell Processes ◽  
Non Coding Rnas ◽  
Per Se ◽  
Dna Regulatory Elements

Although a small number of the vast array of animal long non-coding RNAs (lncRNAs) have known effects on cellular processes examined in vitro, the extent of their contributions to normal cell processes throughout development, differentiation and disease for the most part remains less clear. Phenotypes arising from deletion of an entire genomic locus cannot be unequivocally attributed either to the loss of the lncRNA per se or to the associated loss of other overlapping DNA regulatory elements. The distinction between cis- or trans-effects is also often problematic. We discuss the advantages and challenges associated with the current techniques for studying the in vivo function of lncRNAs in the light of different models of lncRNA molecular mechanism, and reflect on the design of experiments to mutate lncRNA loci. These considerations should assist in the further investigation of these transcriptional products of the genome.

scholarly journals The Role of Non-Coding RNAs in the Regulation of the Proto-Oncogene MYC in Different Types of Cancer

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 921
Author(s):  
Ekaterina Mikhailovna Stasevich ◽  
Matvey Mikhailovich Murashko ◽  
Lyudmila Sergeevna Zinevich ◽  
Denis Eriksonovich Demin ◽  
Anton Markovich Schwartz
Keyword(s):  
Malignant Tumors ◽  
Current Data ◽  
Cellular Processes ◽  
Cell Divisions ◽  
Specific Tumor ◽  
Different Types ◽  
Myc Gene ◽  
Non Coding Rnas ◽  
Tumor Types

Alterations in the expression level of the MYC gene are often found in the cells of various malignant tumors. Overexpressed MYC has been shown to stimulate the main processes of oncogenesis: uncontrolled growth, unlimited cell divisions, avoidance of apoptosis and immune response, changes in cellular metabolism, genomic instability, metastasis, and angiogenesis. Thus, controlling the expression of MYC is considered as an approach for targeted cancer treatment. Since c-Myc is also a crucial regulator of many cellular processes in healthy cells, it is necessary to find ways for selective regulation of MYC expression in tumor cells. Many recent studies have demonstrated that non-coding RNAs play an important role in the regulation of the transcription and translation of this gene and some RNAs directly interact with the c-Myc protein, affecting its stability. In this review, we summarize current data on the regulation of MYC by various non-coding RNAs that can potentially be targeted in specific tumor types.

An Updated Review of the Cross-talk between MicroRNAs and Epigenetic Factors in Cancers

2021 ◽  
Vol 28 ◽  
Author(s):  
Narges Dastmalchi ◽  
Reza Safaralizadeh ◽  
Seyed Mahdi Banan Khojasteh ◽  
Mohammad Reza Sam ◽  
Saeid Latifi-Navid ◽  
...  
Keyword(s):  
Cross Talk ◽  
Transcriptional Networks ◽  
Epigenetic Factors ◽  
Aberrant Expression ◽  
Protein Coding ◽  
Cellular Processes ◽  
Concise Review ◽  
Ample Opportunity ◽  
Histone Modifiers ◽  
The Cross

Background: Growing evidence indicates that miRs have critical activities in adjusting cellular processes, e.g., cell death, proliferation, and cell-cycle. Introduction: This study aimed to provide a concise review of the recent findings regarding tumoral miRs and the cross-talk between miRs and epigenetic factors. Results: Like the protein-coding genes, the expression levels of miRs are mediated by various transcriptional networks. Indeed, the expression of miRs could be epigenetically modulated by DNA methylation factors and histone modifiers. Furthermore, miRs can suppress critical factors, which mediate epigenetic modifications. Besides, miRs have been implicated in cancer development, metastasis, and chemo-resistance. The aberrant expression of miRs and dysregulated modulatory circuits between miRs and epigenetic factors participate in tumor progression. Conclusion: Identifying tumoral miRs can provide ample opportunity to overcome chemo-resistance and bring a forefront treatment for affected patients.

scholarly journals Genetic and Epigenetic Modifiers of Alcoholic Liver Disease

2018 ◽  
Vol 19 (12) ◽  
pp. 3857 ◽  
Author(s):  
Marica Meroni ◽  
Miriam Longo ◽  
Raffaela Rametta ◽  
Paola Dongiovanni
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Complex Disease ◽  
Wide Spectrum ◽  
Association Studies ◽  
Phenotypic Variability ◽  
Genome Wide Association Studies ◽  
Epigenetic Factors ◽  
Excessive Alcohol Consumption

Alcoholic liver disease (ALD), a disorder caused by excessive alcohol consumption is a global health issue. More than two billion people consume alcohol in the world and about 75 million are classified as having alcohol disorders. ALD embraces a wide spectrum of hepatic lesions including steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). ALD is a complex disease where environmental, genetic, and epigenetic factors contribute to its pathogenesis and progression. The severity of alcohol-induced liver disease depends on the amount, method of usage and duration of alcohol consumption as well as on age, gender, presence of obesity, and genetic susceptibility. Genome-wide association studies and candidate gene studies have identified genetic modifiers of ALD that can be exploited as non-invasive biomarkers, but which do not completely explain the phenotypic variability. Indeed, ALD development and progression is also modulated by epigenetic factors. The premise of this review is to discuss the role of genetic variants and epigenetic modifications, with particular attention being paid to microRNAs, as pathogenic markers, risk predictors, and therapeutic targets in ALD.

scholarly journals The Roles of MicroRNA-141 in Human Cancers: From Diagnosis to Treatment

2016 ◽  
Vol 38 (2) ◽  
pp. 427-448 ◽  
Author(s):  
Yanping Gao ◽  
Bing Feng ◽  
Siqi Han ◽  
Kai Zhang ◽  
Jing Chen ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Untranslated Regions ◽  
Messenger Rnas ◽  
Gene Expressions ◽  
Mesenchymal Transition ◽  
Cellular Processes ◽  
Health Impairment ◽  
Non Coding Rnas ◽  
Human Malignant Tumors

Cancer remains one of the most threatening causes of human health impairment, and the mechanisms underlying tumorigenesis have not been completely characterized. MicroRNAs (miRNAs) are a group of endogenous, small (18∼25 nucleotides) non-coding RNAs which negatively regulate gene expressions by directly binding to the 3'-untranslated regions (3'-UTRs) of the target messenger RNAs (mRNAs). Increasing evidence has demonstrated abnormal miRNA profiles and confirmed their involvement in tumor initiation and progression. As one important member of the miR-200 family, microRNA (miR)-141 is aberrantly expressed in many human malignant tumors, participating in various cellular processes including epithelial-mesenchymal transition (EMT), proliferation, migration, invasion, and drug resistance. In the present review, we briefly describe the mechanisms underlying miR-141-mediated tumorigenesis and the possible future of miR-141 as a potential diagnostic and prognostic parameter as well as therapeutic target in clinical applications.

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