METTL1 Promotes Let-7 Microrna Processing Via M7g Methylation
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Nanoliposomal Delivery of Microrna-203 Suppresses Migration of Triple-Negative Breast Cancer Through Distinct Target Suppression
non-coding RNA Article Nanoliposomal Delivery of MicroRNA-203 Suppresses Migration of Triple-Negative Breast Cancer through Distinct Target Suppression Shuxuan Song 1, Kelsey S. Johnson 1, Henry Lujan 2, Sahar H. Pradhan 2 , Christie M. Sayes 2 and Joseph H. Taube 1,* 1 Department of Biology, Baylor University, Waco, TX 76706, USA; [email protected] (S.S.); [email protected] (K.S.J.) 2 Department of Environmental Science, Baylor University, Waco, TX 76706, USA; [email protected] (H.L.); [email protected] (S.H.P.); [email protected] (C.M.S.) * Correspondence: [email protected] Abstract: Triple-negative breast cancers affect thousands of women in the United States and dis- proportionately drive mortality from breast cancer. MicroRNAs are small, non-coding RNAs that negatively regulate gene expression post-transcriptionally by inhibiting target mRNA translation or by promoting mRNA degradation. We have identified that miRNA-203, silenced by epithelial– mesenchymal transition (EMT), is a tumor suppressor and can promote differentiation of breast cancer stem cells. In this study, we tested the ability of liposomal delivery of miR-203 to reverse aspects of breast cancer pathogenesis using breast cancer and EMT cell lines. We show that transla- tionally relevant methods for increasing miR-203 abundance within a target tissue affects cellular Citation: Song, S.; Johnson, K.S.; properties associated with cancer progression. While stable miR-203 expression suppresses LASP1 Lujan, H.; Pradhan, S.H.; Sayes, C.M.; and survivin, nanoliposomal delivery suppresses BMI1, indicating that suppression of distinct mRNA Taube, J.H. Nanoliposomal Delivery target profiles can lead to loss of cancer cell migration. -
Immune Function of Mir-214 and Its Application Prospects As Molecular Marker
Immune function of miR-214 and its application prospects as molecular marker Qiuyuan Wang, Yang Liu, Yiru Wu, Jie Wen and Chaolai Man College of Life Science and Technology, Harbin Normal University, Harbin, China ABSTRACT MicroRNAs are a class of evolutionary conserved non-coding small RNAs that play key regulatory roles at the post-transcriptional level. In recent years, studies have shown that miR-214 plays an important role in regulating several biological processes such as cell proliferation and differentiation, tumorigenesis, inflammation and immunity, and it has become a hotspot in the miRNA field. In this review, the regulatory functions of miR-214 in the proliferation, differentiation and functional activities of immune- related cells, such as dendritic cells, T cells and NK cells, were briefly reviewed. Also, the mechanisms of miR-214 involved in tumor immunity, inflammatory regulation and antivirus were discussed. Finally, the value and application prospects of miR-214 as a molecular marker in inflammation and tumor related diseases were analyzed briefly. We hope it can provide reference for further study on the mechanism and application of miR-214. Subjects Biochemistry, Molecular Biology, Immunology Keywords miR-214, Immune cell, Tumor immunity, Inflammation, Virus, Molecular marker INTRODUCTION MicroRNAs (miRNAs) are a kind of high conserved non-coding small RNAs in evolution that bind to the 30-untranslated region (30-UTR) of target gene mRNA and regulate gene Submitted 18 September 2020 expression at post-transcriptional level. In immune responses, miRNAs act as signal- Accepted 20 January 2021 Published 16 February 2021 regulating molecules after immune-related receptors activation, and affect the expression Corresponding author of immune-related genes, thus extensively participating in various aspects of immune Chaolai Man, [email protected] response (Bosisio et al., 2019; Mehta & Baltimore, 2016). -
ANT2 Shrna Downregulates Mir-19A and Mir-96 Through the PI3K/Akt Pathway and Suppresses Tumor Growth in Hepatocellular Carcinoma Cells
OPEN Experimental & Molecular Medicine (2016) 48, e222; doi:10.1038/emm.2015.126 & 2016 KSBMB. All rights reserved 2092-6413/16 www.nature.com/emm ORIGINAL ARTICLE ANT2 shRNA downregulates miR-19a and miR-96 through the PI3K/Akt pathway and suppresses tumor growth in hepatocellular carcinoma cells Seung Hyun Baik1,3, Jongkuen Lee1,3, Yeong-Shin Lee1,3, Ji-Young Jang1 and Chul-Woo Kim1,2 MicroRNAs (miRNAs) are negative regulators of gene expression, and miRNA deregulation is found in various tumors. We previously reported that suppression of adenine nucleotide translocase 2 (ANT2) by short hairpin RNA (shRNA) inhibits hepatocellular carcinoma (HCC) development by rescuing miR-636 expression. However, the tumor-suppressive mechanisms of ANT2 shRNA are still poorly understood in HCC. Here, we hypothesized that miRNAs that are specifically downregulated by ANT2 shRNA might function as oncomiRs, and we investigated the roles of ANT2 shRNA-regulated miRNAs in the pathogenesis of HCC. Our data show that miR-19a and miR-96, whose expression is regulated by ANT2 suppression, were markedly upregulated in HCC cell lines and clinical samples. Ectopic expression of miR-19a and miR-96 dramatically induced the proliferation and colony formation of hepatoma cells in vitro, whereas inhibition of miR-19a and miR-96 reduced these effects. To investigate the in vivo function, we implanted miR-96-overexpressing HepG2 cells in a xenograft model and demonstrated that the increase in miR-96 promoted tumor growth. We also found that miR-19a and miR-96 inhibited expression of tissue inhibitor of metalloproteinase-2. Taken together, our results suggest that ANT2-regulated miR-19a and miR-96 play an important role in promoting the proliferation of human HCC cells, and the knockdown of ANT2 directly downregulates miR-19a and miR-96, ultimately resulting in the suppression of tumor growth. -
NANOG and LIN28 Dramatically Improve Human Cell Reprogramming
© 2019. Published by The Company of Biologists Ltd | Biology Open (2019) 8, bio047225. doi:10.1242/bio.047225 RESEARCH ARTICLE NANOG and LIN28 dramatically improve human cell reprogramming by modulating LIN41 and canonical WNT activities Ling Wang, Yue Su, Chang Huang, Yexuan Yin, Alexander Chu, Alec Knupp and Young Tang* ABSTRACT (Hussein et al., 2014). The first transcriptional change occurs at the Human cell reprogramming remains extremely inefficient and the early reprogramming stage, with cells undergoing mesenchymal-to- underlying mechanisms by different reprogramming factors are epithelial transition (MET) for iPSC colony formation (Hussein elusive. We found that NANOG and LIN28 (NL) synergize to improve et al., 2014; Li et al., 2010; Samavarchi-Tehrani et al., 2010). This OCT4, SOX2, KLF4 and MYC (OSKM)-mediated reprogramming by stage is followed by the second wave that occurs during maturation ∼76-fold and shorten reprogramming latency by at least 1 week. This and stabilization, when the pluripotency regulatory network is synergy is inhibited by GLIS1 but reinforced by an inhibitor of the activated and stabilized in reprogrammed cells (Buganim et al., 2012; histone methyltransferase DOT1L (iDOT1L) to a ∼127-fold increase in Golipour et al., 2012; Hussein et al., 2014; Polo et al., 2012; TRA-1-60-positive (+) iPSC colonies. Mechanistically, NL serve as the Samavarchi-Tehrani et al., 2010). In human cells, the early-to-middle main drivers of reprogramming in cell epithelialization, the expression reprogramming stages are characterized by multiple waves of lineage- of Let-7 miRNA target LIN41, and the activation of canonical WNT/β- related gene activation in the order of developmental reversal, with CATENIN signaling, which can be further enhanced by iDOT1L MET occurring at the middle-to-late-reprogramming stage along with treatment. -
Elevated Circulating Microrna-122 Is Associated with Obesity and Insulin Resistance in Young Adults
R Wang, J Hong, Y Cao and miR-122, obesity and insulin 172:3 291–300 Clinical Study others resistance Elevated circulating microRNA-122 is associated with obesity and insulin resistance in young adults Rui Wang1,*, Jie Hong1,*, Yanan Cao1,*, Juan Shi1, Weiqiong Gu1, Guang Ning1,2, Yifei Zhang1 and Weiqing Wang1 1Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrinology and Metabolism, Shanghai Key Laboratory for Endocrine Tumors and E-Institutes of Shanghai Universities, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China and 2Laboratory for Endocrine and Metabolism, Institute of Health Sciences, Correspondence Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School should be addressed of Medicine, Shanghai 200025, China to W Wang *(R Wang, J Hong and Y Cao contributed equally to this work) Email [email protected] Abstract Objective: MicroRNAs (miRNAs) are involved in the regulation of adiposity, but functional studies have yielded inconclusive results. Examining the associations of circulating miRNAs levels with obesity and insulin sensitivity in humans may lead to improved insights. Design and methods: Serum samples collected from 112 obese and control subjects (50.0% men) were randomly divided and combined into four pools (28 samples in each obese or control pool). The genome-wide circulating miRNA profiles were detected via microarray. Elevated miR-122 was selected and validated in individual serum samples from 123 obese (46.7% men) and 107 control (50.0% men) young adults. Associations between circulating miR-122 levels and parameters related to adiposity, insulin resistance, lipid profiles and hepatic enzymes were further assessed. -
A Lncrna/Lin28/Mirlet7 Axis Coupled to DNA Methylation Fine Tunes the Dynamics of a Cell State Transition
bioRxiv preprint doi: https://doi.org/10.1101/131110; this version posted April 26, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Li, M.A. et al A lncRNA/Lin28/Mirlet7 axis coupled to DNA methylation fine tunes the dynamics of a cell state transition Meng Amy Li1*,2,#, Paulo P. Amaral3, Priscilla Cheung2, Jan H. Bergmann4,9, Masaki Kinoshita1, Tüzer Kalkan1, Meryem Ralser1, Sam Robson3, Ferdinand von Meyenn5, Maike Paramor1, Fengtang Yang6, Caifu Chen7, Jennifer Nichols1, David L. Spector4, Tony Kouzarides3, Lin He2,#, Austin Smith1,8,# 1. Wellcome Trust - Medical Research Council Stem Cell Institute, Tennis Court Road, University of Cambridge, Cambridge, CB2 1QR, UK 2. Division of Cellular and Developmental Biology, Department of Molecular and Cellular Biology, University of California Berkeley, Berkeley, California 94705, USA 3. The Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QN, UK 4. Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA 5. Babraham Institute, Babraham, Cambridge, CB22 3AT 6. Wellcome Trust Sanger Institute, Genome Campus, Hinxton, CB10 1SA, UK 7. Integrated DNA Technologies, 200 Chesapeake Drive, Redwood City, CA 94063, USA. 8. Department of Biochemistry, University of Cambridge, CB2 1QW, UK 9. Current address: Agenus inc., Hochbergerstrasse 60C, 4057 Basel, Switzerland *. Current address. # . Correspondence: [email protected], [email protected] and [email protected] Lead contact: Austin Smith Summary Execution of pluripotency requires progression from the naïve status represented by mouse embryonic stem cells (ESCs) to a condition poised for lineage specification. -
Microrna Pharmacoepigenetics: Posttranscriptional Regulation Mechanisms Behind Variable Drug Disposition and Strategy to Develop More Effective Therapy
1521-009X/44/3/308–319$25.00 http://dx.doi.org/10.1124/dmd.115.067470 DRUG METABOLISM AND DISPOSITION Drug Metab Dispos 44:308–319, March 2016 Copyright ª 2016 by The American Society for Pharmacology and Experimental Therapeutics Minireview MicroRNA Pharmacoepigenetics: Posttranscriptional Regulation Mechanisms behind Variable Drug Disposition and Strategy to Develop More Effective Therapy Ai-Ming Yu, Ye Tian, Mei-Juan Tu, Pui Yan Ho, and Joseph L. Jilek Department of Biochemistry & Molecular Medicine, University of California Davis School of Medicine, Sacramento, California Received September 30, 2015; accepted November 12, 2015 Downloaded from ABSTRACT Knowledge of drug absorption, distribution, metabolism, and excre- we review the advances in miRNA pharmacoepigenetics including tion (ADME) or pharmacokinetics properties is essential for drug the mechanistic actions of miRNAs in the modulation of Phase I and development and safe use of medicine. Varied or altered ADME may II drug-metabolizing enzymes, efflux and uptake transporters, and lead to a loss of efficacy or adverse drug effects. Understanding the xenobiotic receptors or transcription factors after briefly introducing causes of variations in drug disposition and response has proven the characteristics of miRNA-mediated posttranscriptional gene dmd.aspetjournals.org critical for the practice of personalized or precision medicine. The regulation. Consequently, miRNAs may have significant influence rise of noncoding microRNA (miRNA) pharmacoepigenetics and on drug disposition and response. Therefore, research on miRNA pharmacoepigenomics has come with accumulating evidence sup- pharmacoepigenetics shall not only improve mechanistic under- porting the role of miRNAs in the modulation of ADME gene standing of variations in pharmacotherapy but also provide novel expression and then drug disposition and response. -
Microrna-155 Modulates Bile Duct Inflammation by Targeting the Suppressor of Cytokine Signaling 1 in Biliary Atresia
nature publishing group Basic Science Investigation | Articles MicroRNA-155 modulates bile duct inflammation by targeting the suppressor of cytokine signaling 1 in biliary atresia Rui Zhao1, Rui Dong1, Yifan Yang1, Yuqing Wang1, Jin Ma2, Jiang Wang1, Hao Li1 and Shan Zheng1 BACKGROUND: Biliary atresia (BA) is an etiologically etiology and pathogenesis of BA remains largely unknown. A perplexing disease, manifested by neonatal cholestasis, leading hypothesis for the pathogenesis of BA is a virus repeated cholangitis, and progressive biliary fibrosis. MiR-155 infection-initiated bile duct injury (possibly prenatal), which has been implicated to modulate the immune response, is then followed by an exaggerated inflammatory or which contributes to biliary injury. However, its potential role autoimmune response targeting the bile duct epithelium. in the pathogenesis of BA has not been addressed so far. This ultimately results in progressive bile duct injury, METHODS: The microRNA changes from BA patients and obliteration, and secondary biliary cirrhosis (3,4). controls were identified via microarray. The immunomodula- Gene expression is primarily regulated at a post- tory function of miR-155 was investigated via cell transfection transcriptional level by microRNAs (miRNAs), which exert and reporter assay. The lentiviral vector pL-miR-155 inhibitor their function by targeting complementary mRNA molecules, was transfected into a mouse model to investigate its thus inhibiting their translation by binding to the 3′ role in BA. untranslated region (UTR) (5). Many miRNAs have been RESULTS: The expression of miR-155 in livers of BA patients reported to be differentially expressed in autoimmune diseases was significantly increased, and an inverse correlation and consequently may have a pivotal role in the regulation of between miR-155 and suppressor of cytokine signaling 1 both immune responses and autoimmunity. -
An Ontogenetic Switch Drives the Positive and Negative Selection of B Cells
An ontogenetic switch drives the positive and negative selection of B cells Xijin Xua, Mukta Deobagkar-Lelea, Katherine R. Bulla, Tanya L. Crockforda, Adam J. Meadb, Adam P. Cribbsc, David Simsc, Consuelo Anzilottia, and Richard J. Cornalla,1 aMedical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS Oxford, United Kingdom; bMedical Research Council Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS Oxford, United Kingdom; and cMedical Research Council, Weatherall Institute of Molecular Medicine, Centre for Computational Biology, Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS Oxford, United Kingdom Edited by Michael Reth, University of Freiburg, Freiburg, Germany, and approved January 6, 2020 (received for review September 3, 2019) + Developing B cells can be positively or negatively selected by self- BM HSCs increased CD5 B-1a B cell development (15), while antigens, but the mechanisms that determine these outcomes are expression of let-7b in FL pro-B cells blocked the development of incompletely understood. Here, we show that a B cell intrinsic B-1 B cells (17). These findings support the notion of hard-wired switch between positive and negative selection during ontogeny differences during ontogeny, but possibly downstream of the HSC is determined by a change from Lin28b to let-7 gene expression. commitment stage. Ectopic expression of a Lin28b transgene in murine B cells restored Several lines of evidence also suggest that B-1 B cells can un- the positive selection of autoreactive B-1 B cells by self-antigen in dergo positive selection, which is linked to their B cell receptor adult bone marrow. -
Análise Integrativa De Perfis Transcricionais De Pacientes Com
UNIVERSIDADE DE SÃO PAULO FACULDADE DE MEDICINA DE RIBEIRÃO PRETO PROGRAMA DE PÓS-GRADUAÇÃO EM GENÉTICA ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas Ribeirão Preto – 2012 ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas Tese apresentada à Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo para obtenção do título de Doutor em Ciências. Área de Concentração: Genética Orientador: Prof. Dr. Eduardo Antonio Donadi Co-orientador: Prof. Dr. Geraldo A. S. Passos Ribeirão Preto – 2012 AUTORIZO A REPRODUÇÃO E DIVULGAÇÃO TOTAL OU PARCIAL DESTE TRABALHO, POR QUALQUER MEIO CONVENCIONAL OU ELETRÔNICO, PARA FINS DE ESTUDO E PESQUISA, DESDE QUE CITADA A FONTE. FICHA CATALOGRÁFICA Evangelista, Adriane Feijó Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas. Ribeirão Preto, 2012 192p. Tese de Doutorado apresentada à Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo. Área de Concentração: Genética. Orientador: Donadi, Eduardo Antonio Co-orientador: Passos, Geraldo A. 1. Expressão gênica – microarrays 2. Análise bioinformática por module maps 3. Diabetes mellitus tipo 1 4. Diabetes mellitus tipo 2 5. Diabetes mellitus gestacional FOLHA DE APROVAÇÃO ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas. -
LIN28B Promotes the Development of Neuroendocrine Prostate Cancer
LIN28B promotes the development of neuroendocrine prostate cancer Jessica M. Lovnicki, … , Martin Gleave, Xuesen Dong J Clin Invest. 2020. https://doi.org/10.1172/JCI135373. Research In-Press Preview Oncology Graphical abstract Find the latest version: https://jci.me/135373/pdf LIN28B promotes the development of neuroendocrine prostate cancer Jessica Lovnicki1, *, Yu Gan1, 2, *, Tingting Feng1, 3, Yinan Li1, Ning Xie1, Chia-Hao Ho1, Ahn Lee1, Xufeng Chen4, Lucia Nappi1, Bo Han3, Ladan Fazli1, Jiaoti Huang4, Martin Gleave1, Xuesen Dong1 1) The Vancouver Prostate Centre, Department of Urologic Sciences, University of British Columbia, Vancouver, British Columbia, Canada 2) Department of Urology, Xiangya Hospital, Central South University, Changsha, Hunan Province, China 3) The Key Laboratory of Experimental Teratology, Ministry of Education, and Department of Pathology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong Province, China 4) Department of Pathology, Duke University School of Medicine, Durham, North Carolina, USA *) The authors equally contribute to this work. Corresponding author: Xuesen Dong, Ph.D. 2660 Oak Street, Vancouver, British Columbia, Canada V6H 3Z6, Tel: 604-875-4111 Fax: 604-875-5654 Email: [email protected] Disclosure Statement: The authors have declared that no conflict of interest exists. 1 Abstract Therapy-induced neuroendocrine prostate cancer (t-NEPC) is a highly aggressive subtype of prostate cancer with poor patient survival. Emerging evidence indicates that t-NEPC can develop when prostate adenocarcinoma cells acquire cancer stem-like cell signaling in the presence of androgen receptor inhibition, followed by re-differentiation toward neuroendocrine lineage and subsequent t-NEPC progression. Whether the stem-like signaling is controlled by the core pluripotency stem cell genes (e.g., LIN28 and SOX2) remains unknown. -
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Published OnlineFirst April 9, 2015; DOI: 10.1158/0008-5472.CAN-14-2215 Cancer Tumor and Stem Cell Biology Research Lin28B/Let-7 Regulates Expression of Oct4 and Sox2 and Reprograms Oral Squamous Cell Carcinoma Cells to a Stem-like State Chian-Shiu Chien1, Mong-Lien Wang2,3, Pen-Yuan Chu4,5, Yuh-Lih Chang2,6, Wei-Hsiu Liu7, Cheng-Chia Yu8, Yuan-Tzu Lan3,6, Pin-I. Huang3,9, Yi-Yen Lee3,9, Yi-Wei Chen3,9, Wen-Liang Lo1,10, and Shih-Hwa Chiou2,3,4,6,11 Abstract Lin28, a key factor for cellular reprogramming and generation HMGA2 and suppressed their expression, whereas ARID3B and of induced pluripotent stem cell (iPSC), makes a critical con- HMGA2 increased the transcription of Oct4 and Sox2, respec- tribution to tumorigenicity by suppressing Let-7. However, it is tively, through promoter binding. Chromatin immunoprecipi- unclear whether Lin28 is involved in regulating cancer stem–like tation assays revealed a direct association between ARID3B and cells (CSC), including in oral squamous carcinoma cells aspecific ARID3B-binding sequence in the Oct4 promoter. (OSCC). In this study, we demonstrate a correlation between Notably, by modulating Oct4/Sox2 expression, the Lin28B–Let7 high levels of Lin28B, Oct4, and Sox2, and a high percentage of pathway not only regulated stemness properties in OSCC but þ þ CD44 ALDH1 CSC in OSCC. Ectopic Lin28B expression also determined the efficiency by which normal human oral À À in CD44 ALDH1 /OSCC cells was sufficient to enhance keratinocytes could be reprogrammed to iPSC. Clinically, a Oct4/Sox2 expression and CSC properties, whereas Let7 co- Lin28Bhigh-Let7low expression pattern was highly correlated with overexpression effectively reversed these phenomena.