English

MINCR is a MYC-induced lncRNA able to modulate MYC’s transcriptional network in Burkitt lymphoma cells

2015 
Despite the established role of the transcription factor MYC in cancer, little is known about the impact of a new class of transcriptional regulators, the long noncoding RNAs (lncRNAs), on MYC ability to influence the cellular transcriptome. Here, we have intersected RNA-sequencing data from two MYC-inducible cell lines and a cohort of 91 B-cell lymphomas with or without genetic variants resulting in MYC overexpression. We identified 13 lncRNAs differentially expressed in IG-MYC-positive Burkitt lymphoma and regulated in the same direction by MYC in the model cell lines. Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Differential gene expression analysis after RNAi showed a significant enrichment of cell cycle genes among the genes down-regulated after MINCR knockdown. Interestingly, these genes are enriched in MYC binding sites in their promoters, suggesting that MINCR acts as a modulator of the MYC transcriptional program. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A and B and chromatin licensing and DNA replication factor 1 may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.
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    [ { "id": "2049972", "title": "Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma", "abstract": "Burkitt lymphoma (BL) is the most common B-cell lymphoma in children. Within the International Cancer Genome Consortium (ICGC), we performed whole genome and transcriptome sequencing of 39 sporadic BL. Here, we unravel interaction of structural, mutational, and transcriptional changes, which contribute to MYC oncogene dysregulation together with the pathognomonic IG-MYC translocation. Moreover, by mapping IGH translocation breakpoints, we provide evidence that the precursor of at least a subset of BL is a B-cell poised to express IGHA. We describe the landscape of mutations, structural variants, and mutational processes, and identified a series of driver genes in the pathogenesis of BL, which can be targeted by various mechanisms, including IG-non MYC translocations, germline and somatic mutations, fusion transcripts, and alternative splicing. Burkitt lymphoma (BL) is the most common pediatric B-cell lymphoma. Here, within the International Cancer Genome Consortium, the authors performed whole genome and transcriptome sequencing of 39 sporadic BL, describing the landscape of mutations, structural variants, and mutational processes that underpin this disease how alterations on different cellular levels cooperate in deregulating key pathways and complexes.", "source_url": "https://www.nature.com/articles/s41467-019-08578-3", "doc_type": 4, "year": 2019, "issue": 1, "volume": 10, "first_page": 1, "last_page": 19, "citation_count": 2, "reference_count": 13, "venue": { "id": 2110000199, "name": "NATURE COMMUNICATIONS", "abbr": "" }, "author": [ { "id": 1000139278, "name": "Cristina Lopez" }, { "id": 1001206668, "name": "Kortine Kleinheinz" }, { "id": 1001370235, "name": "Sietse M. Aukema" }, { "id": 1001312430, "name": "Marius Rohde" }, { "id": 1001293933, "name": "Stephan H. Bernhart" }, { "id": 1001206667, "name": "Daniel Hübschmann" }, { "id": 1001312561, "name": "Rabea Wagener" }, { "id": 1001312529, "name": "Umut H. Toprak" }, { "id": 1000927968, "name": "Francesco Raimondi" }, { "id": 1001312258, "name": "Markus Kreuz" }, { "id": 1001182094, "name": "Sebastian M. Waszak" }, { "id": 1001892453, "name": "Zhiqin Huang" }, { "id": 1001182080, "name": "Lina Sieverling" }, { "id": 1001276528, "name": "Nagarajan Paramasivam" }, { "id": 1001987845, "name": "Julian Seufert" }, { "id": 1001312503, "name": "Stephanie Sungalee" }, { "id": 1001193367, "name": "Robert B. Russell" }, { "id": 1001987846, "name": "Julia Bausinger" }, { "id": 1001312257, "name": "Helene Kretzmer" }, { "id": 1001311963, "name": "Ole Ammerpohl" }, { "id": 1001311994, "name": "Anke K. Bergmann" }, { "id": 1001205523, "name": "Hans Binder" }, { "id": 1001192605, "name": "Arndt Borkhardt" }, { "id": 1001249013, "name": "Benedikt Brors" }, { "id": 1001312062, "name": "Alexander Claviez" }, { "id": 1001293936, "name": "Gero Doose" }, { "id": 1001182007, "name": "Lars Feuerbach" }, { "id": 1001312160, "name": "Andrea Haake" }, { "id": 1001370229, "name": "Martin-Leo Hansmann" }, { "id": 1001918217, "name": "Jessica Hoell" }, { "id": 1001312195, "name": "Michael Hummel" }, { "id": 1001182036, "name": "Jan O. Korbel" }, { "id": 1001312271, "name": "Chris Lawerenz" }, { "id": 1001312280, "name": "Dido Lenze" }, { "id": 1001209672, "name": "Bernhard Radlwimmer" }, { "id": 1001162754, "name": "Julia Richter" }, { "id": 1001162449, "name": "Philip Rosenstiel" }, { "id": 1001176809, "name": "Andreas Rosenwald" }, { "id": 1001312458, "name": "Markus B. Schilhabel" }, { "id": 1001260013, "name": "Harald Stein" }, { "id": 1001312500, "name": "Stephan Stilgenbauer" }, { "id": 1001271864, "name": "Peter F. Stadler" }, { "id": 1001312507, "name": "Monika Szczepanowski" }, { "id": 1001987847, "name": "Marc A. Weniger" }, { "id": 1001190483, "name": "Marc Zapatka" }, { "id": 1001197337, "name": "Roland Eils" }, { "id": 1001190495, "name": "Peter Lichter" }, { "id": 1001312291, "name": "Markus Loeffler" }, { "id": 1000224526, "name": "Peter Möller" }, { "id": 1001370232, "name": "Lorenz Trümper" }, { "id": 1001312250, "name": "Wolfram Klapper" }, { "id": 1001228402, "name": "Susanne Wagner" }, { "id": 1001370222, "name": "Gesine Richter" }, { "id": 1001370192, "name": "Jürgen Eils" }, { "id": 1001370223, "name": "Jules Kerssemakers" }, { "id": 1001370224, "name": "Christina Jaeger-Schmidt" }, { "id": 1001370225, "name": "Ingrid Scholz" }, { "id": 1001312011, "name": "Christoph Borst" }, { "id": 1001987848, "name": "Friederike Braulke" }, { "id": 1001370226, "name": "Martin Dreyling" }, { "id": 1001370227, "name": "Sonja Eberth" }, { "id": 1001200348, "name": "Hermann Einsele" }, { "id": 1001370228, "name": "Norbert Frickhofen" }, { "id": 1001312161, "name": "Siegfried Haas" }, { "id": 1001312231, "name": "Dennis Karsch" }, { "id": 1001987849, "name": "Nicole Klepl" }, { "id": 1001312251, "name": "Michael Kneba" }, { "id": 1001370230, "name": "Jasmin Lisfeld" }, { "id": 1001312310, "name": "Luisa Mantovani-Löffler" }, { "id": 1001284349, "name": "German Ott" }, { "id": 1001370231, "name": "Christina Stadler" }, { "id": 1001312496, "name": "Peter Staib" }, { "id": 1001199138, "name": "Thorsten Zenz" }, { "id": 1001312260, "name": "Dieter Kube" }, { "id": 1001370234, "name": "Ulrike Kostezka" }, { "id": 1001350008, "name": "Vera Binder" }, { "id": 1001370236, "name": "Ellen Leich" }, { "id": 1001370237, "name": "Inga Nagel" }, { "id": 1001370238, "name": "Jordan Pischimariov" }, { "id": 1000594910, "name": "Stefan Schreiber" }, { "id": 1001370239, "name": "Inga Vater" }, { "id": 1001370240, "name": "Lydia Hopp" }, { "id": 1001370241, "name": "David Langenberger" }, { "id": 1001370242, "name": "Maciej Rosolowski" }, { "id": 1001271857, "name": "Steve Hoffmann" }, { "id": 1001312264, "name": "Ralf Küppers" }, { "id": 1001312030, "name": "Birgit Burkhardt" }, { "id": 1001206689, "name": "Matthias Schlesner" }, { "id": 1001223411, "name": "Reiner Siebert" } ], "field": [], "cite": [ { "name": "GB/T 7714", "text": "Lopez Cristina, Kleinheinz Kortine, Aukema Sietse M., et al. Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma[J]. NATURE COMMUNICATIONS, 2019, 10(1): 1-19." }, { "name": "MLA", "text": "Lopez, Cristina, et al. \"Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma\" NATURE COMMUNICATIONS., vol. 10, no. 1, 2019, pp. 1-19." }, { "name": "APA", "text": "Lopez Cristina, Kleinheinz Kortine, Aukema Sietse M., Rohde Marius, Bernhart Stephan H., Hübschmann Daniel, ... & Kreuz Markus (2019). Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma. NATURE COMMUNICATIONS, 10(1), 1-19." }, { "name": "BibTeX", "text": "@inproceedings{Acemap2049972,\n title=\"Genomic and transcriptomic changes complement each other in the pathogenesis of sporadic Burkitt lymphoma\",\n author=\"Cristina {Lopez} and Kortine {Kleinheinz} and {Sietse M. Aukema} and Marius {Rohde} and {Stephan H. Bernhart} and {Daniel Hübschmann} and Rabea {Wagener} and {Umut H. Toprak} and Francesco {Raimondi} and Markus {Kreuz} and {Sebastian M. Waszak} and Zhiqin {Huang} and Lina {Sieverling} and Nagarajan {Paramasivam} and Julian {Seufert} and Stephanie {Sungalee} and {Robert B. Russell} and Julia {Bausinger} and Helene {Kretzmer} and Ole {Ammerpohl} and {Anke K. Bergmann} and Hans {Binder} and Arndt {Borkhardt} and Benedikt {Brors} and Alexander {Claviez} and Gero {Doose} and Lars {Feuerbach} and Andrea {Haake} and {Martin-Leo Hansmann} and Jessica {Hoell} and Michael {Hummel} and {Jan O. Korbel} and Chris {Lawerenz} and Dido {Lenze} and Bernhard {Radlwimmer} and Julia {Richter} and Philip {Rosenstiel} and Andreas {Rosenwald} and {Markus B. Schilhabel} and Harald {Stein} and Stephan {Stilgenbauer} and {Peter F. Stadler} and Monika {Szczepanowski} and {Marc A. Weniger} and Marc {Zapatka} and Roland {Eils} and Peter {Lichter} and Markus {Loeffler} and {Peter Möller} and {Lorenz Trümper} and Wolfram {Klapper} and Susanne {Wagner} and Gesine {Richter} and {Jürgen Eils} and Jules {Kerssemakers} and {Christina Jaeger-Schmidt} and Ingrid {Scholz} and Christoph {Borst} and Friederike {Braulke} and Martin {Dreyling} and Sonja {Eberth} and Hermann {Einsele} and Norbert {Frickhofen} and Siegfried {Haas} and Dennis {Karsch} and Nicole {Klepl} and Michael {Kneba} and Jasmin {Lisfeld} and {Luisa Mantovani-Löffler} and German {Ott} and Christina {Stadler} and Peter {Staib} and Thorsten {Zenz} and Dieter {Kube} and Ulrike {Kostezka} and Vera {Binder} and Ellen {Leich} and Inga {Nagel} and Jordan {Pischimariov} and Stefan {Schreiber} and Inga {Vater} and Lydia {Hopp} and David {Langenberger} and Maciej {Rosolowski} and Steve {Hoffmann} and {Ralf Küppers} and Birgit {Burkhardt} and Matthias {Schlesner} and Reiner {Siebert}\",\n journal=\"NATURE COMMUNICATIONS\",\n volume=\"10\",\n number=\"1\",\n pages=\"1--19\",\n url=\"https://www.acemap.info/paper/2049972\",\n year=\"2019\"\n}" } ] }, { "id": "2304484", "title": "Human skin long noncoding RNA WAKMAR1 regulates wound healing by enhancing keratinocyte migration", "abstract": "An increasing number of studies reveal the importance of long noncoding RNAs (lncRNAs) in gene expression control underlying many physiological and pathological processes. However, their role in skin wound healing remains poorly understood. Our study focused on a skin-specific lncRNA, LOC105372576, whose expression was increased during physiological wound healing. In human nonhealing wounds, however, its level was significantly lower compared with normal wounds under reepithelialization. We characterized LOC105372576 as a nuclear-localized, RNAPII-transcribed, and polyadenylated lncRNA. In keratinocytes, its expression was induced by TGF-β signaling. Knockdown of LOC105372576 and activation of its endogenous transcription, respectively, reduced and increased the motility of keratinocytes and reepithelialization of human ex vivo skin wounds. Therefore, LOC105372576 was termed “wound and keratinocyte migration-associated lncRNA 1” (WAKMAR1). Further study revealed that WAKMAR1 regulated a network of protein-coding genes important for cell migration, most of which were under the control of transcription factor E2F1. Mechanistically, WAKMAR1 enhanced E2F1 expression by interfering with E2F1 promoter methylation through the sequestration of DNA methyltransferases. Collectively, we have identified a lncRNA important for keratinocyte migration, whose deficiency may be involved in the pathogenesis of chronic wounds.", "source_url": "https://www.pnas.org/content/116/19/9443", "doc_type": 4, "year": 2019, "issue": 19, "volume": 116, "first_page": 9443, "last_page": 9452, "citation_count": 1, "reference_count": 10, "venue": { "id": 2110000201, "name": "PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA", "abbr": "" }, "author": [ { "id": 1000692160, "name": "Dongqing Li" }, { "id": 1001701495, "name": "Lara Kular" }, { "id": 1002489215, "name": "Manika Vij" }, { "id": 1002489216, "name": "Eva K. Herter" }, { "id": 1000435770, "name": "Xi Li" }, { "id": 1001350094, "name": "Aoxue Wang" }, { "id": 1002489217, "name": "Tongbin Chu" }, { "id": 1002489218, "name": "Maria-Alexandra Toma" }, { "id": 1000331834, "name": "Letian Zhang" }, { "id": 1000906529, "name": "Eleni Liapi" }, { "id": 1001482312, "name": "Ana Mota" }, { "id": 1001983441, "name": "Lennart Blomqvist" }, { "id": 1002489219, "name": "Irène Gallais Sérézal" }, { "id": 1002489220, "name": "Ola Rollman" }, { "id": 1001166572, "name": "Jakob D. Wikstrom" }, { "id": 1001305136, "name": "Magda Bienko" }, { "id": 1002372281, "name": "David Berglund" }, { "id": 1001166575, "name": "Mona Ståhle" }, { "id": 1002489221, "name": "Pehr Sommar" }, { "id": 1001195777, "name": "Maja Jagodic" }, { "id": 1001166576, "name": "Ning Xu Landén" } ], "field": [ { "id": 2001237175, "name": "Centipede bite" } ], "cite": [ { "name": "GB/T 7714", "text": "Li Dongqing, Kular Lara, Vij Manika, et al. Human skin long noncoding RNA WAKMAR1 regulates wound healing by enhancing keratinocyte migration[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2019, 116(19): 9443-9452." }, { "name": "MLA", "text": "Li, Dongqing, et al. \"Human skin long noncoding RNA WAKMAR1 regulates wound healing by enhancing keratinocyte migration\" PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA., vol. 116, no. 19, 2019, pp. 9443-9452." }, { "name": "APA", "text": "Li Dongqing, Kular Lara, Vij Manika, Herter Eva K., Li Xi, Wang Aoxue, ... & Liapi Eleni (2019). Human skin long noncoding RNA WAKMAR1 regulates wound healing by enhancing keratinocyte migration. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 116(19), 9443-9452." }, { "name": "BibTeX", "text": "@inproceedings{Acemap2304484,\n title=\"Human skin long noncoding RNA WAKMAR1 regulates wound healing by enhancing keratinocyte migration\",\n author=\"Dongqing {Li} and Lara {Kular} and Manika {Vij} and {Eva K. Herter} and Xi {Li} and Aoxue {Wang} and Tongbin {Chu} and {Maria-Alexandra Toma} and Letian {Zhang} and Eleni {Liapi} and Ana {Mota} and Lennart {Blomqvist} and {Irène Gallais Sérézal} and Ola {Rollman} and {Jakob D. Wikstrom} and Magda {Bienko} and David {Berglund} and {Mona Ståhle} and Pehr {Sommar} and Maja {Jagodic} and {Ning Xu Landén}\",\n journal=\"PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA\",\n volume=\"116\",\n number=\"19\",\n pages=\"9443--9452\",\n url=\"https://www.acemap.info/paper/2304484\",\n year=\"2019\"\n}" } ] }, { "id": "1628321", "title": "Integrative analysis identifies lincRNAs up- and downstream of neuroblastoma driver genes", "abstract": "Long intergenic non-coding RNAs (lincRNAs) are emerging as integral components of signaling pathways in various cancer types. In neuroblastoma, only a handful of lincRNAs are known as upstream regulators or downstream effectors of oncogenes. Here, we exploit RNA sequencing data of primary neuroblastoma tumors, neuroblast precursor cells, neuroblastoma cell lines and various cellular perturbation model systems to define the neuroblastoma lincRNome and map lincRNAs up- and downstream of neuroblastoma driver genes MYCN, ALK and PHOX2B. Each of these driver genes controls the expression of a particular subset of lincRNAs, several of which are associated with poor survival and are differentially expressed in neuroblastoma tumors compared to neuroblasts. By integrating RNA sequencing data from both primary tumor tissue and cancer cell lines, we demonstrate that several of these lincRNAs are expressed in stromal cells. Deconvolution of primary tumor gene expression data revealed a strong association between stromal cell composition and driver gene status, resulting in differential expression of these lincRNAs. We also explored lincRNAs that putatively act upstream of neuroblastoma driver genes, either as presumed modulators of driver gene activity, or as modulators of effectors regulating driver gene expression. This analysis revealed strong associations between the neuroblastoma lincRNAs MIAT and MEG3 and MYCN and PHOX2B activity or expression. Together, our results provide a comprehensive catalogue of the neuroblastoma lincRNome, highlighting lincRNAs up- and downstream of key neuroblastoma driver genes. This catalogue forms a solid basis for further functional validation of candidate neuroblastoma lincRNAs.", "source_url": "https://www.nature.com/articles/s41598-019-42107-y", "doc_type": 4, "year": 2019, "issue": 1, "volume": 9, "first_page": 1, "last_page": 13, "citation_count": 0, "reference_count": 17, "venue": { "id": 2110000208, "name": "SCIENTIFIC REPORTS", "abbr": "" }, "author": [ { "id": 1001359975, "name": "Dries Rombaut" }, { "id": 1001359976, "name": "Hua-Sheng Chiu" }, { "id": 1001228054, "name": "Bieke Decaesteker" }, { "id": 1001359977, "name": "Celine Everaert" }, { "id": 1001359978, "name": "Nurten Yigit" }, { "id": 1001359979, "name": "Agathe Peltier" }, { "id": 1001170872, "name": "Isabelle Janoueix-Lerosey" }, { "id": 1001192591, "name": "Christoph Bartenhagen" }, { "id": 1000954633, "name": "Matthias Fischer" }, { "id": 1000095716, "name": "Stephen Roberts" }, { "id": 1001194183, "name": "Nicky D’Haene" }, { "id": 1001216903, "name": "Katleen De Preter" }, { "id": 1001228062, "name": "Frank Speleman" }, { "id": 1001228060, "name": "Geertrui Denecker" }, { "id": 1001217874, "name": "Pavel Sumazin" }, { "id": 1001228058, "name": "Jo Vandesompele" }, { "id": 1001316620, "name": "Steve Lefever" }, { "id": 1001216902, "name": "Pieter Mestdagh" } ], "field": [ { "id": 2015533717, "name": "Glomus tumour" }, { "id": 2008621301, "name": "Glomangioma" }, { "id": 2018252668, "name": "Penile cancer" }, { "id": 2004556151, "name": "Appendix cancer" } ], "cite": [ { "name": "GB/T 7714", "text": "Rombaut Dries, Chiu Hua-Sheng, Decaesteker Bieke, et al. Integrative analysis identifies lincRNAs up- and downstream of neuroblastoma driver genes[J]. SCIENTIFIC REPORTS, 2019, 9(1): 1-13." }, { "name": "MLA", "text": "Rombaut, Dries, et al. \"Integrative analysis identifies lincRNAs up- and downstream of neuroblastoma driver genes\" SCIENTIFIC REPORTS., vol. 9, no. 1, 2019, pp. 1-13." }, { "name": "APA", "text": "Rombaut Dries, Chiu Hua-Sheng, Decaesteker Bieke, Everaert Celine, Yigit Nurten, Peltier Agathe, ... & Roberts Stephen (2019). Integrative analysis identifies lincRNAs up- and downstream of neuroblastoma driver genes. SCIENTIFIC REPORTS, 9(1), 1-13." }, { "name": "BibTeX", "text": "@inproceedings{Acemap1628321,\n title=\"Integrative analysis identifies lincRNAs up- and downstream of neuroblastoma driver genes\",\n author=\"Dries {Rombaut} and {Hua-Sheng Chiu} and Bieke {Decaesteker} and Celine {Everaert} and Nurten {Yigit} and Agathe {Peltier} and {Isabelle Janoueix-Lerosey} and Christoph {Bartenhagen} and Matthias {Fischer} and Stephen {Roberts} and {Nicky D’Haene} and Katleen De {Preter} and Frank {Speleman} and Geertrui {Denecker} and Pavel {Sumazin} and Jo {Vandesompele} and Steve {Lefever} and Pieter {Mestdagh}\",\n journal=\"SCIENTIFIC REPORTS\",\n volume=\"9\",\n number=\"1\",\n pages=\"1--13\",\n url=\"https://www.acemap.info/paper/1628321\",\n year=\"2019\"\n}" } ] }, { "id": "2594204", "title": "Portraying breast cancers with long noncoding RNAs", "abstract": "Evidence is emerging that long noncoding RNAs (lncRNAs) may play a role in cancer development, but this role is not yet clear. We performed a genome-wide transcriptional survey to explore the lncRNA landscape across 995 breast tissue samples. We identified 215 lncRNAs whose genes are aberrantly expressed in breast tumors, as compared to normal samples. Unsupervised hierarchical clustering of breast tumors on the basis of their lncRNAs revealed four breast cancer subgroups that correlate tightly with PAM50-defined mRNA-based subtypes. Using multivariate analysis, we identified no less than 210 lncRNAs prognostic of clinical outcome. By analyzing the coexpression of lncRNA genes and protein-coding genes, we inferred potential functions of the 215 dysregulated lncRNAs. We then associated subtype-specific lncRNAs with key molecular processes involved in cancer. A correlation was observed, on the one hand, between luminal A–specific lncRNAs and the activation of phosphatidylinositol 3-kinase, fibroblast growth factor, and transforming growth factor–β pathways and, on the other hand, between basal-like–specific lncRNAs and the activation of epidermal growth factor receptor (EGFR)–dependent pathways and of the epithelial-to-mesenchymal transition. Finally, we showed that a specific lncRNA, which we called CYTOR, plays a role in breast cancer. We confirmed its predicted functions, showing that it regulates genes involved in the EGFR/mammalian target of rapamycin pathway and is required for cell proliferation, cell migration, and cytoskeleton organization. Overall, our work provides the most comprehensive analyses for lncRNA in breast cancers. Our findings suggest a wide range of biological functions associated with lncRNAs in breast cancer and provide a foundation for functional investigations that could lead to new therapeutic approaches.", "source_url": "https://advances.sciencemag.org/content/2/9/e1600220", "doc_type": 4, "year": 2016, "issue": 9, "volume": 2, "first_page": 0, "last_page": 0, "citation_count": 6, "reference_count": 9, "venue": { "id": 2110000198, "name": "SCIENCE ADVANCES", "abbr": "" }, "author": [ { "id": 1002789547, "name": "Olivier Van Grembergen" }, { "id": 1001976429, "name": "Martin Bizet" }, { "id": 1002789548, "name": "Eric J. de Bony" }, { "id": 1001331298, "name": "Emilie Calonne" }, { "id": 1001976439, "name": "Pascale Putmans" }, { "id": 1001357986, "name": "Sylvain Brohée" }, { "id": 1001263954, "name": "Catharina Olsen" }, { "id": 1001732568, "name": "Mingzhou Guo" }, { "id": 1001763747, "name": "Gianluca Bontempi" }, { "id": 1001258015, "name": "Christos Sotiriou" }, { "id": 1001331299, "name": "Matthieu Defrance" }, { "id": 1001331300, "name": "François Fuks" } ], "field": [ { "id": 2018252668, "name": "Penile cancer" }, { "id": 2004556151, "name": "Appendix cancer" }, { "id": 2011716103, "name": "Halichondrin B" }, { "id": 2017571735, "name": "Migrastatin" } ], "cite": [ { "name": "GB/T 7714", "text": "Grembergen Olivier Van, Bizet Martin, Bony Eric J. de, et al. Portraying breast cancers with long noncoding RNAs[J]. SCIENCE ADVANCES, 2016, 2(9)." }, { "name": "MLA", "text": "Grembergen, Olivier Van, et al. \"Portraying breast cancers with long noncoding RNAs\" SCIENCE ADVANCES., vol. 2, no. 9, 2016." }, { "name": "APA", "text": "Grembergen Olivier Van, Bizet Martin, Bony Eric J. de, Calonne Emilie, Putmans Pascale, Brohée Sylvain, ... & Sotiriou Christos (2016). Portraying breast cancers with long noncoding RNAs. SCIENCE ADVANCES, 2(9)." }, { "name": "BibTeX", "text": "@inproceedings{Acemap2594204,\n title=\"Portraying breast cancers with long noncoding RNAs\",\n author=\"Olivier Van {Grembergen} and Martin {Bizet} and {Eric J. de Bony} and Emilie {Calonne} and Pascale {Putmans} and {Sylvain Brohée} and Catharina {Olsen} and Mingzhou {Guo} and Gianluca {Bontempi} and Christos {Sotiriou} and Matthieu {Defrance} and {François Fuks}\",\n journal=\"SCIENCE ADVANCES\",\n volume=\"2\",\n number=\"9\",\n url=\"https://www.acemap.info/paper/2594204\",\n year=\"2016\"\n}" } ] }, { "id": "2261791", "title": "Expression of the Long Non-Coding RNA HOTAIR Correlates with Disease Progression in Bladder Cancer and Is Contained in Bladder Cancer Patient Urinary Exosomes", "abstract": "Exosomes are 30-150nM membrane-bound secreted vesicles that are readily isolated from biological fluids such as urine (UEs). Exosomes contain proteins, micro RNA (miRNA), messenger RNA (mRNA), and long non-coding RNA (lncRNA) from their cells of origin. Although miRNA, protein and lncRNA have been isolated from serum as potential biomarkers for benign and malignant disease, it is unknown if lncRNAs in UEs from urothelial bladder cancer (UBC) patients can serve as biomarkers. lncRNAs are > 200 nucleotide long transcripts that do not encode protein and play critical roles in tumor biology. As the number of recognized tumor-associated lncRNAs continues to increase, there is a parallel need to include lncRNAs into biomarker discovery and therapeutic target algorithms. The lncRNA HOX transcript antisense RNA (HOTAIR) has been shown to facilitate tumor initiation and progression and is associated with poor prognosis in several cancers. The importance of HOTAIR in cancer biology has sparked interest in using HOTAIR as a biomarker and potential therapeutic target. Here we show HOTAIR and several tumor-associated lncRNAs are enriched in UEs from UBC patients with high-grade muscle-invasive disease (HGMI pT2-pT4). Knockdown of HOTAIR in UBC cell lines reduces in vitro migration and invasion. Importantly, loss of HOTAIR expression in UBC cell lines alters expression of epithelial-to-mesenchyme transition (EMT) genes including SNAI1, TWIST1, ZEB1, ZO1, MMP1 LAMB3, and LAMC2. Finally, we used RNA-sequencing to identify four additional lncRNAs enriched in UBC patient UEs. These data, suggest that UE-derived lncRNA may potentially serve as biomarkers and therapeutic targets.", "source_url": "https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0147236", "doc_type": 4, "year": 2016, "issue": 1, "volume": 11, "first_page": 0, "last_page": 0, "citation_count": 5, "reference_count": 7, "venue": { "id": 2110000215, "name": "PLOS ONE", "abbr": "" }, "author": [ { "id": 1002383847, "name": "Claudia Berrondo" }, { "id": 1002028272, "name": "Jonathan Flax" }, { "id": 1002383848, "name": "Victor Kucherov" }, { "id": 1002383849, "name": "Aisha Siebert" }, { "id": 1002383850, "name": "Thomas Osinski" }, { "id": 1001527665, "name": "Alex Rosenberg" }, { "id": 1002243288, "name": "Christopher Fucile" }, { "id": 1002383851, "name": "Samuel Richheimer" }, { "id": 1002383852, "name": "Carla J. Beckham" } ], "field": [ { "id": 2018252668, "name": "Penile cancer" }, { "id": 2046479603, "name": "MicA RNA" }, { "id": 2010169572, "name": "Mapatumumab" }, { "id": 2011716103, "name": "Halichondrin B" }, { "id": 2029468943, "name": "Physostome" }, { "id": 2004556151, "name": "Appendix cancer" }, { "id": 2017571735, "name": "Migrastatin" } ], "cite": [ { "name": "GB/T 7714", "text": "Berrondo Claudia, Flax Jonathan, Kucherov Victor, et al. Expression of the Long Non-Coding RNA HOTAIR Correlates with Disease Progression in Bladder Cancer and Is Contained in Bladder Cancer Patient Urinary Exosomes[J]. PLOS ONE, 2016, 11(1)." }, { "name": "MLA", "text": "Berrondo, Claudia, et al. \"Expression of the Long Non-Coding RNA HOTAIR Correlates with Disease Progression in Bladder Cancer and Is Contained in Bladder Cancer Patient Urinary Exosomes\" PLOS ONE., vol. 11, no. 1, 2016." }, { "name": "APA", "text": "Berrondo Claudia, Flax Jonathan, Kucherov Victor, Siebert Aisha, Osinski Thomas, Rosenberg Alex, ... & Beckham Carla J. (2016). Expression of the Long Non-Coding RNA HOTAIR Correlates with Disease Progression in Bladder Cancer and Is Contained in Bladder Cancer Patient Urinary Exosomes. PLOS ONE, 11(1)." }, { "name": "BibTeX", "text": "@inproceedings{Acemap2261791,\n title=\"Expression of the Long Non-Coding RNA HOTAIR Correlates with Disease Progression in Bladder Cancer and Is Contained in Bladder Cancer Patient Urinary Exosomes\",\n author=\"Claudia {Berrondo} and Jonathan {Flax} and Victor {Kucherov} and Aisha {Siebert} and Thomas {Osinski} and Alex {Rosenberg} and Christopher {Fucile} and Samuel {Richheimer} and {Carla J. Beckham}\",\n journal=\"PLOS ONE\",\n volume=\"11\",\n number=\"1\",\n url=\"https://www.acemap.info/paper/2261791\",\n year=\"2016\"\n}" } ] }, { "id": "2322727", "title": "MINCR is not a MYC-induced lncRNA", "abstract": "", "source_url": "https://www.pnas.org/content/113/5/E496", "doc_type": 4, "year": 2016, "issue": 5, "volume": 113, "first_page": 0, "last_page": 0, "citation_count": 1, "reference_count": 4, "venue": { "id": 2110000201, "name": "PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA", "abbr": "" }, "author": [ { "id": 1002494767, "name": "Jonathan R. Hart" }, { "id": 1002084704, "name": "Marc S. Weinberg" }, { "id": 1001752275, "name": "Kevin V. Morris" }, { "id": 1001418279, "name": "Thomas C. Roberts" }, { "id": 1001488576, "name": "Kim D. Janda" }, { "id": 1002523366, "name": "Amanda L. Garner" }, { "id": 1001493822, "name": "Peter K. Vogt" } ], "field": [], "cite": [ { "name": "GB/T 7714", "text": "Hart Jonathan R., Weinberg Marc S., Morris Kevin V., et al. MINCR is not a MYC-induced lncRNA[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2016, 113(5)." }, { "name": "MLA", "text": "Hart, Jonathan R., et al. \"MINCR is not a MYC-induced lncRNA\" PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA., vol. 113, no. 5, 2016." }, { "name": "APA", "text": "Hart Jonathan R., Weinberg Marc S., Morris Kevin V., Roberts Thomas C., Janda Kim D., Garner Amanda L., ... & Vogt Peter K. (2016). MINCR is not a MYC-induced lncRNA. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 113(5)." }, { "name": "BibTeX", "text": "@inproceedings{Acemap2322727,\n title=\"MINCR is not a MYC-induced lncRNA\",\n author=\"{Jonathan R. Hart} and {Marc S. Weinberg} and {Kevin V. Morris} and {Thomas C. Roberts} and {Kim D. Janda} and {Amanda L. Garner} and {Peter K. Vogt}\",\n journal=\"PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA\",\n volume=\"113\",\n number=\"5\",\n url=\"https://www.acemap.info/paper/2322727\",\n year=\"2016\"\n}" } ] }, { "id": "2404005", "title": "Reply to Hart et al.: MINCR and MYC: More than expression correlation", "abstract": "", "source_url": "https://www.pnas.org/content/113/5/E498", "doc_type": 4, "year": 2016, "issue": 5, "volume": 113, "first_page": 0, "last_page": 0, "citation_count": 0, "reference_count": 2, "venue": { "id": 2110000201, "name": "PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA", "abbr": "" }, "author": [ { "id": 1001293936, "name": "Gero Doose" }, { "id": 1001271857, "name": "Steve Hoffmann" }, { "id": 1002576224, "name": "Ingram Iaccarino" } ], "field": [], "cite": [ { "name": "GB/T 7714", "text": "Doose Gero, Hoffmann Steve, Iaccarino Ingram, et al. Reply to Hart et al.: MINCR and MYC: More than expression correlation[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2016, 113(5)." }, { "name": "MLA", "text": "Doose, Gero, et al. \"Reply to Hart et al.: MINCR and MYC: More than expression correlation\" PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA., vol. 113, no. 5, 2016." }, { "name": "APA", "text": "Doose Gero, Hoffmann Steve, & Iaccarino Ingram (2016). Reply to Hart et al.: MINCR and MYC: More than expression correlation. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 113(5)." }, { "name": "BibTeX", "text": "@inproceedings{Acemap2404005,\n title=\"Reply to Hart et al.: MINCR and MYC: More than expression correlation\",\n author=\"Gero {Doose} and Steve {Hoffmann} and Ingram {Iaccarino}\",\n journal=\"PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA\",\n volume=\"113\",\n number=\"5\",\n url=\"https://www.acemap.info/paper/2404005\",\n year=\"2016\"\n}" } ] } ]