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Exercise regulates shelterin genes and micrornas implicated in ageing in Thoroughbred horses

PFLUGERS ARCHIV-EUROPEAN JOUrnaL OF PHYSIOLOGY 2022年第11期474卷 1159-1169页

作者： Mandal, Shama Denham, Michele M. Spencer, Sarah J. Denham, Joshua RMIT Univ Sch Hlth & Biomed Sci Melbourne Vic Australia Jubilee Stud Freshwater Creek Vic Australia RMIT Univ ARC Ctr Excellence Nanoscale Biophoton Melbourne Vic Australia Univ Southern Queensland Sch Hlth & Med Sci Ipswich Qld 4305 Australia Univ New England Sch Sci & Technol Armidale NSW Australia

Ageing causes a gradual deterioration of bodily functions and telomere degradation. Excessive telomere shortening leads to cellular senescence and decreases tissue vitality. Six proteins, called shelterin, protect telomere integrity and control telomere length through telomerase-dependent mechanisms. Exercise training appears to maintain telomeres in certain somatic cells, although the underlying molecular mechanisms are incompletely understood. Here, we examined the influence of a single bout of vigorous exercise training on leukocyte telomerase reverse transcriptase (TERT) and shelterin gene expression, and the abundance of three micrornas (mirnas) implicated in biological ageing (mirna-143, -223 and -486-5p) in an elite athlete and large animal model, Thoroughbred horses. Gene and mirna expression were analysed using primer-based and TaqMan Assay qPCR. Leukocyte TRF1, TRF2 and POT1 expression were all significantly increased whilst miR-223 and miR-486-5p were decreased immediately after vigorous exercise (all p < 0.05), and tended to return to baseline levels 24 h after training. Relative to the young horses (similar to 3.9 years old), middle-aged horses (similar to 14.8 years old) exhibited reduced leukocyte TERT gene expression, and increased POT1 and miR-223 abundance (all p < 0.05). These data demonstrate that genes transcribing key components of the shelterin-telomere complex are influenced by ageing and dynamically regulated by a single bout of vigorous exercise in a large, athletic mammal - Thoroughbred horses. Our findings also implicate TERT and shelterin gene transcripts as potential targets of miR-223 and miR-486-5p, which are modulated by exercise and may have a role in the telomere maintenance and genomic stability associated with long-term aerobic training.

关键词： Telomere TERT non-coding rna mirna Equine

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Integrated regulation of chondrogenic differentiation in mesenchymal stem cells and differentiation of cancer cells

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CANCER CELL INTErnaTIONAL 2022年第1期22卷 1-13页

作者： Yang, Xiaohui Tian, Shifeng Fan, Linlin Niu, Rui Yan, Man Chen, Shuo Zheng, Minying Zhang, Shiwu Nankai Univ Sch Med Tianjin 300071 Peoples R China Tianjin Med Univ Grad Sch Tianjin 300070 Peoples R China Tianjin Univ Tradit Chinese Med Grad Sch Dept Pathol Tianjin 301617 Peoples R China Tianjin Union Med Ctr Dept Colorectal Surg Tianjin Peoples R China Tianjin Union Med Ctr Dept Pathol Tianjin 300071 Peoples R China

Chondrogenesis is the formation of chondrocytes and cartilage tissues and starts with mesenchymal stem cell (MSC) recruitment and migration, condensation of progenitors, chondrocyte differentiation, and maturation. The chondrogenic differentiation of MSCs depends on co-regulation of many exogenous and endogenous factors including specific microenvironmental signals, non-coding rnas, physical factors existed in culture condition, etc. Cancer stem cells (CSCs) exhibit self-renewal capacity, pluripotency and cellular plasticity, which have the potential to differentiate into post-mitotic and benign cells. Accumulating evidence has shown that CSCs can be induced to differentiate into various benign cells including adipocytes, fibrocytes, osteoblast, and so on. Retinoic acid has been widely used in the treatment of acute promyelocytic leukemia. Previous study confirmed that polyploid giant cancer cells, a type of cancer stem-like cells, could differentiate into adipocytes, osteocytes, and chondrocytes. In this review, we will summarize signaling pathways and cytokines in chondrogenic differentiation of MSCs. Understanding the molecular mechanism of chondrogenic differentiation of CSCs and cancer cells may provide new strategies for cancer treatment.

关键词： Chondrogenic differentiation Mesenchymal stem cells Signaling pathway non-coding rna Cancer stem cell Polyploidy giant cancer cells

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A unique glimpse into the crosstalk between different epigenetic mechanisms in porcine embryonic development^†

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BIOLOGY OF REPRODUCTION 2022年第6期107卷 1411-1424页

作者： Gan, Jianyu Zhang, Xin Lu, Yongchang Wu, Zhenfang Cai, Gengyuan Hong, Linjun South China Agr Univ Coll Anim Sci Natl Engn Res Ctr Breeding Swine Ind Guangzhou Peoples R China South China Agr Univ Coll Anim Sci Guangdong Prov Key Lab Agroanim Genom & Mol Breed Guangzhou Peoples R China State Key Lab Conservat & Utilizat Subtrop Agrobi Guangzhou Peoples R China

In this review, four epigenetic modifications (DNA methylation, histone modification, non-coding rna function, and chromatin accessibility) were described in porcine embryonic development, and the possible crosstalk between them was explored in order to provide references for further understanding and studying the role of epigenetic modification in embryonic development. The pig is an excellent animal model for simulating human physiology and a major animal for meat production and xenotransplantation. Therefore, researching porcine embryonic development is crucial for studying human reproductive diseases and improving litter size in commercial pigs. Embryonic development in pigs occurs under a complex regulatory mechanism, in which epigenetic regulatory mechanisms play an essential role. Recently, studies on the effects of epigenetic modifications on embryonic development have been conducted at different developmental stages and in different cell lines. Increasing evidence suggests that a certain amount of crosstalk exists between different epigenetic modifications. This review describes four regulatory mechanisms of epigenetics involved in porcine embryonic development: DNA methylation, histone modification, non-coding rna function, and chromatin accessibility, and explores the possible crosstalk between them.

关键词： pig embryo DNA methylation histone modification non-coding rna chromatin accessibility

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Downregulation of nc886 contributes to prostate cancer cell invasion and TGFβ1-induced EMT

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Genes & Diseases 2022年第4期9卷 1086-1098页

作者： Ronghui Yang Lingkun Zuo Hui Ma Ying Zhou Ping Zhou Liyong Wang Miao Wang Mahrukh Latif Lu Kong Department of Biochemistry and Molecular Biology Capital Medical UniversityBeijing 100069PR China Biomedical Engineering Institute of Capital Medical University Capital Medical UniversityBeijing 100069PR China Department of Pathology Beijing Friendship HospitalThe Second Clinical Medical College of Capital Medical UniversityBeijing 100050PR China Department of Nuclear Medicine Fourth Hospital of Hebei Medical UniversityShijiazhuangHebei 050010PR China

Epithelial-to-mesenchymal transition (EMT) activation is important in cancer progression and metastasis. Evidence indicates that nc886 is a representative Pol III gene that processes microrna products via Dicer and further downregulates its target gene transforming growth factor- β1 (TGF-β1), which is the most prominent inducer of EMT in prostate cancer (PC). Consistent with the previous literature, we found that nc886 downregulation was strongly associated with metastatic behavior and showed worse outcomes in PC patients. However, little is known about the association between nc886 and the EMT signaling pathway. We developed a PC cell model with stable overexpression of nc886 and found that nc886 changed cellular morphology and drove MET. The underlying mechanism may be related to its promotion of SNAIL protein degradation via ubiquitination, but not to its neighboring genes, TGFβ-induced protein (TGFBI) and SMAD5, which are Pol II-transcribed. TGF-β1 also override nc886 promotion of MET via transient suppression the transcription of nc886, promotion of TGFBI or increase in SMAD5 phosphorylation. Both nc886 inhibition and TGFBI activation occur regardless of their methylation status. The literature suggests that MYC inhibition by TGF-β1 is attributed to nc886 downregulation. We incidentally identified MYC-associated zinc finger protein (MAZ) as a suppressive transcription factor of TGFBI, which is controlled by TGF-β1. We elucidate a new mechanism of TGF-β1 differential control of Pol II and the transcription of its neighboring Pol III gene and identify a new EMT unit consisting of nc886 and its neighboring genes.

关键词： EMT MET non-coding rna Prostate cancer TGF-β1

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The Small non-coding Vault rna1-1 Acts as a Riboregulator of Autophagy

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CELL 2019年第5期176卷 1054-+页

作者： Horos, Rastislav Buescher, Magdalena Kleinendorst, Rozemarijn Alleaume, Anne-Marie Tarafder, Abul K. Schwarzl, Thomas Dziuba, Dmytro Tischer, Christian Zielonka, Elisabeth M. Adak, Asli Castello, Alfredo Huber, Wolfgang Sachse, Carsten Hentze, Matthias W. European Mol Biol Lab Meyerhofstr 1 D-69117 Heidelberg Germany Univ Oxford Dept Biochem South Parks Rd Oxford OX1 3QU England Ernst Ruska Ctr Microscopy & Spect Electrons ER C Wilhem Johnen Str D-52425 Julich Germany

Vault rnas (vtrna) are small non-coding rnas transcribed by rna polymerase III found in many eukaryotes. Although they have been linked to drug resistance, apoptosis, and viral replication, their molecular functions remain unclear. Here, we show that vault rnas directly bind the autophagy receptor sequestosome-1/p62 in human and murine cells. Overexpression of human vtrna1-1 inhibits, while its antisense LNA-mediated knockdown enhances p62-dependent autophagy. Starvation of cells reduces the steady-state and p62-bound levels of vault rna1-1 and induces autophagy. Mechanistically, p62 mutants that fail to bind vtrnas display increased p62 homo-oligomerization and augmented interaction with autophagic effectors. Thus, vtrna1-1 directly regulates selective autophagy by binding p62 and interference with oligomerization, a critical step of p62 function. Our data uncover a striking example of the potential of rna to control protein functions directly, as previously recognized for protein-protein interactions and post-translational modifications.

关键词： vault rna autophagy p62 sequestosome-1 vtrna1-1 vtrna starvation non-coding rna SQSTM1

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CircPVT1: a pivotal circular node intersecting Long non-coding-PVT1 and c-MYC oncogenic signals

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MOLECULAR CANCER 2022年第1期21卷 1-15页

作者： Palcau, Alina Catalina Canu, Valeria Donzelli, Sara Strano, Sabrina Pulito, Claudio Blandino, Giovanni IRCCS Regina Elena Natl Canc Inst Oncogen & Epigenet Unit Via Elio Chianesi 53 I-00144 Rome Italy IRCCS Regina Elena Natl Canc Inst SAFU Lab Dept Res Adv Diagnost & Technol Innovat Rome Italy

The role of circular rnas in oncogenesis has begun to be widely studied in recent years, due to the significant impact that these molecules have in disease pathogenesis, as well as their potential for the future of innovative therapies. Moreover, due to their characteristically circular shape, circular rnas are very resistant molecules to rna degradation whose levels are easily assessed in body fluids. Accordingly, they represent an opportunity for the discovery of new diagnostic and prognostic markers in a wide range of diseases. Among circular rnas, circPVT1 is a rather peculiar one that originates from the circularization of the exon 2 of the PVT1 gene that encodes a pro-tumorigenic long non-coding rna named lncPVT1. There are a few examples of circular rnas that derive from a locus producing another non-coding rna. Despite their apparent transcriptional independence, which occurs using two different promoters, a possible synergistic effect in tumorigenesis cannot be excluded considering that both have been reported to correlate with the oncogenic phenotype. This complex mechanism of regulation appears to also be controlled by c-MYC. Indeed, the PVT1 locus is located only 53 Kb downstream c-MYC gene, a well-known oncogene that regulates the expression levels of about 15% of all genes. Here, we review circPVT1 origin and biogenesis highlighting the most important mechanisms through which it plays a fundamental role in oncogenesis, such as the well-known sponge activity on micrornas, as well as its paradigmatic interactome link with lncPVT1 and c-MYC expression.

关键词： non-coding rna circular rna circPVT1 PVT1 c-MYC sponge peptide

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non-coding rnas in cardiovascular cell biology and atherosclerosis

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CARDIOVASCULAR RESEARCH 2019年第12期115卷 1732-1756页

作者： Fasolo, Francesca Di Gregoli, Karina Maegdefessel, Lars Johnson, Jason L. Tech Univ Munich Klinikum Rechts Isar Dept Vasc & Endovasc Surg Biedersteiner Str 29 D-80802 Munich Germany Univ Bristol Bristol Med Sch Lab Cardiovasc Pathol Bristol BS2 8HW Avon England Karolinska Inst Ctr Mol Med L8 03 Mol Vasc Med S-17176 Stockholm Sweden Munich Heart Alliance German Ctr Cardiovasc Res DZHK Partner Site Munich Munich Germany

Atherosclerosis underlies the predominant number of cardiovascular diseases and remains a leading cause of morbidity and mortality worldwide. The development, progression and formation of clinically relevant atherosclerotic plaques involves the interaction of distinct and over-lapping mechanisms which dictate the roles and actions of multiple resident and recruited cell types including endothelial cells, vascular smooth muscle cells, and monocyte/macrophages. The discovery of non-coding rnas (ncrnas) including micrornas, long non-coding rnas, and circular rnas, and their identification as key mechanistic regulators of mrna and protein expression has piqued interest in their potential contribution to atherosclerosis. Accruing evidence has revealed ncrnas regulate pivotal cellular and molecular processes during all stages of atherosclerosis including cell invasion, growth, and survival;cellular uptake and efflux of lipids, expression and release of pro- and anti-inflammatory intermediaries, and proteolytic balance. The expression profile of ncrnas within atherosclerotic lesions and the circulation have been determined with the aim of identifying individual or clusters of ncrnas which may be viable therapeutic targets alongside deployment as biomarkers of atherosclerotic plaque progression. Consequently, numerous in vivo studies have been convened to determine the effects of moderating the function or expression of select ncrnas in well-characterized animal models of atherosclerosis. Together, clinicopathological findings and studies in animal models have elucidated the multifaceted and frequently divergent effects ncrnas impose both directly and indirectly on the formation and progression of atherosclerosis. From these findings' potential novel therapeutic targets and strategies have been discovered which may pave the way for further translational studies and possibly taken forward for clinical application.

关键词： Atherosclerosis non-coding rna microrna Vascular smooth muscle cells Endothelial cells Macrophages

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Dissecting non-coding rna mechanisms in cellulo by Single-molecule High-Resolution Localization and Counting

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METHODS 2013年第2期63卷 188-199页

作者： Pitchiaya, Sethuramasundaram Krishnan, Vishalakshi Custer, Thomas C. Walter, Nils G. Univ Michigan Single Mol Anal Real Time SMART Ctr Ann Arbor MI 48109 USA Univ Michigan Single Mol Anal Grp Dept Chem Ann Arbor MI 48109 USA Univ Michigan Program Chem Biol Ann Arbor MI 48109 USA

non-coding rnas (ncrnas) recently were discovered to outnumber their protein-coding counterparts, yet their diverse functions are still poorly understood. Here we report on a method for the intracellular Single-molecule High-Resolution Localization and Counting (iSHiRLoC) of micrornas (mirnas), a conserved, ubiquitous class of regulatory ncrnas that controls the expression of over 60% of all mammalian protein coding genes post-transcriptionally, by a mechanism shrouded by seemingly contradictory observations. We present protocols to execute single particle tracking (SPT) and single-molecule counting of functional microinjected, fluorophore-labeled mirnas and thereby extract diffusion coefficients and molecular stoichiometries of micro-ribonucleoprotein (miRNP) complexes from living and fixed cells, respectively. This probing of mirnas at the single molecule level sheds new light on the intracellular assembly/disassembly of miRNPs, thus beginning to unravel the dynamic nature of this important gene regulatory pathway and facilitating the development of a parsimonious model for their obscured mechanism of action. (C) 2013 Elsevier Inc. All rights reserved.

关键词： rna silencing microrna non-coding rna Single molecule microscopy Single particle tracking

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Long non-coding rnas in breast cancer metastasis

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non-coding rna RESEARCH 2020年第4期5卷 208-218页

作者： Mondal, Priya Meeran, Syed Musthapa CSIR Cent Food Technol Res Inst Dept Biochem Lab Canc Epigenet Mysore 570020 Karnataka India Acad Sci & Innovat Res AcSIR Ghaziabad 201002 India

Breast cancer is the leading cause of cancer-related death among women. Recurrence of primary tumor and metastasis to distant body parts are major causes of breast cancer-associated mortality. The 5-year survival rate for women with metastatic breast cancer is only 25-30%. Breast cancer metastasis is a series of processes involved with EMT, invasion, loss of cell to cell adhesion, alteration in cell phenotype, extravasation, microenvironment of the tumor, and colonization to the secondary sites. Epigenetic modification is involved in the transformation of the distant stromal cell into a secondary tumor. Lncrnas, are one the key epigenetic modifiers, are the largest endogenous non-coding rnas with approximate base-pair lengths from 200 nt to 100 kb. Lncrna plays a crucial role in breast cancer metastasis by sponging mirna, by degrading or silencing specific mrna, or else by targeting the enzymes and microprocessor subunits involved in the biogenesis of mirna. Lncrna also alters the expression of several genes involved in breast cancer metastasis and modulating different cell signaling pathways. The goal of this review is to provide a better understanding of the role of lncrna in the regulation of breast cancer metastasis. We also summarized some of the key lncrnas that regulate the genes and signaling pathways involved in breast cancer invasion and metastasis.

关键词： Breast cancer Metastasis non-coding rna EMT Long non-coding rna Signaling pathway

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Large-scale study of long non-coding rna functions based on structure and expression features

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Science China(Life Sciences) 2013年第10期56卷 953-959页

作者： ZHAO Yi WANG Jian CHEN XiaoWei LUO HaiTao ZHAO YunJie XIAO Yi CHEN RenSheng Bioinformatics Research Group Advanced Computing Research LaboratoryInstitute of Computing TechnologyChinese Academy ofSciences Department of Physics Huazhong University of Science and Technology Laboratory of Bioinformatics and Non-coding RNA Institute of BiophysicsChinese Academy of Sciences

Mammals and other complex organisms can transcribe an abundance of long non-coding rnas(lncrnas)that fulfill a wide variety of regulatory roles in many biological *** roles,including as scaffolds and as guides for protein-coding genes,mainly depend on the structure and expression level of *** this review,we focus on the current methods for analyzing lncrna structure and expression,which is basic but necessary information for in-depth,large-scale analysis of lncrna functions.

关键词： non-coding rna structure expression function

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