The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition

Bibliographic Details
Main Author: Mateos, Cristina Oliveira
Publication Date: 2019
Other Authors: Castillo, Anaís Sánchez, Soler, Marta, Guardia, Aida Obiols, Piñeyro, David, Sastre, Raquel Boque, Cervantes, Maria E. Calleja, Moura, Manuel Castro de, Cardús, Anna Martínez, Rubio, Teresa, Pelletier, Joffrey, Iniesta, Maria Martínez, Martín, David Herrero, Tirado, Oscar M., Gentilella, Antonio, Villanueva, Alberto, Esteller, Manel, Vallve, Maria de Lourdes Farre, Guil, Sonia
Format: Article
Language: eng
Source: Repositório Institucional da FIOCRUZ (ARCA)
DOI: 10.1038/s41467-019-11910-6
Download full: https://arca.fiocruz.br/handle/icict/37085
Summary: Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.
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spelling Mateos, Cristina OliveiraCastillo, Anaís SánchezSoler, MartaGuardia, Aida ObiolsPiñeyro, DavidSastre, Raquel BoqueCervantes, Maria E. CallejaMoura, Manuel Castro deCardús, Anna MartínezRubio, TeresaPelletier, JoffreyIniesta, Maria MartínezMartín, David HerreroTirado, Oscar M.Gentilella, AntonioVillanueva, AlbertoEsteller, ManelVallve, Maria de Lourdes FarreGuil, Sonia2019-11-14T18:43:18Z2019-11-14T18:43:18Z2019MATEOS, Cristina Oliveira et al. The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition. Nature Communications, v. 10, p. 1-18, 2019.2041-1723https://arca.fiocruz.br/handle/icict/3708510.1038/s41467-019-11910-6engNature ResearchPseudogenesTumoresProteína HMGA2PrognósticoPseudogenesNeoplasmsHMGA2 ProteinPrognosisThe transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibitioninfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleBellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain / Carlos III Institute of Health. Centro de Investigación Biomédica en Red de Cáncer. Madrid, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain / Cardiff School of Biosciences. Cardiff University. Wales, UK.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Laboratory of Cancer Metabolism. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Laboratory of Cancer Metabolism. Barcelona, Catalonia, Spain.IDIBELLL’Hospitalet de Llobregat. Program Against Cancer Therapeutic Resistance. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Sarcoma Research Group. Barcelona, Catalonia, Spain.Carlos III Institute of Health. Centro de Investigación Biomédica en Red de Cáncer. Madrid, Spain / Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Sarcoma Research Group. Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Laboratory of Cancer Metabolism. Barcelona, Catalonia, Spain / University of Barcelona. Faculty of Pharmacy. Department of Biochemistry and Physiology. Barcelona, Catalonia, Spain.IDIBELLL’Hospitalet de Llobregat. Program Against Cancer Therapeutic Resistance.Barcelona, Catalonia, Spain.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain / Carlos III Institute of Health. Centro de Investigación Biomédica en Red de Cáncer. Madrid, Spain / University of Barcelona. School of Medicine and Health Sciences. Physiological Sciences Department. Barcelona, Catalonia, Spain / Institució Catalana de Recerca i Estudis Avançats. Barcelona, Catalonia, Spain / Josep Carreras Leukaemia Research Institute Badalona. Barcelona, Catalonia, Spain.IDIBELL,L’Hospitalet de Llobregat. Program Against Cancer Therapeutic Resistance.Barcelona, Catalonia, Spain / Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Laboratório de Patologia Experimental. Salvador, BA, Brasil.Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain / Josep Carreras Leukaemia Research Institute. Badalona, Barcelona, Catalonia, Spain.One largely unknown question in cell biology is the discrimination between inconsequential and functional transcriptional events with relevant regulatory functions. Here, we find that the oncofetal HMGA2 gene is aberrantly reexpressed in many tumor types together with its antisense transcribed pseudogene RPSAP52. RPSAP52 is abundantly present in the cytoplasm, where it interacts with the RNA binding protein IGF2BP2/IMP2, facilitating its binding to mRNA targets, promoting their translation by mediating their recruitment on polysomes and enhancing proliferative and self-renewal pathways. Notably, downregulation of RPSAP52 impairs the balance between the oncogene LIN28B and the tumor suppressor let-7 family of miRNAs, inhibits cellular proliferation and migration in vitro and slows down tumor growth in vivo. In addition, high levels of RPSAP52 in patient samples associate with a worse prognosis in sarcomas. Overall, we reveal the roles of a transcribed pseudogene that may display properties of an oncofetal master regulator in human cancers.info:eu-repo/semantics/openAccessreponame:Repositório Institucional da FIOCRUZ (ARCA)instname:Fundação Oswaldo Cruz (FIOCRUZ)instacron:FIOCRUZLICENSElicense.txtlicense.txttext/plain; charset=utf-82991https://arca.fiocruz.br/bitstreams/85b9485f-c75a-43bf-a0e5-0ea33c2f5f35/download5a560609d32a3863062d77ff32785d58MD51falseAnonymousREADORIGINALOliveira, M. The_transcribed....pdfOliveira, M. The_transcribed....pdfapplication/pdf2639421https://arca.fiocruz.br/bitstreams/7045b9de-ba72-4c43-8c07-6cd524977210/download651f2a2ec223a67a3e7d3fac77d43034MD52trueAnonymousREADTEXTOliveira, M. The_transcribed....pdf.txtOliveira, M. 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dc.title.none.fl_str_mv The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition
title The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition
spellingShingle The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition
Mateos, Cristina Oliveira
Pseudogenes
Tumores
Proteína HMGA2
Prognóstico
Pseudogenes
Neoplasms
HMGA2 Protein
Prognosis
title_short The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition
title_full The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition
title_fullStr The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition
title_full_unstemmed The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition
title_sort The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition
author Mateos, Cristina Oliveira
author_facet Mateos, Cristina Oliveira
Castillo, Anaís Sánchez
Soler, Marta
Guardia, Aida Obiols
Piñeyro, David
Sastre, Raquel Boque
Cervantes, Maria E. Calleja
Moura, Manuel Castro de
Cardús, Anna Martínez
Rubio, Teresa
Pelletier, Joffrey
Iniesta, Maria Martínez
Martín, David Herrero
Tirado, Oscar M.
Gentilella, Antonio
Villanueva, Alberto
Esteller, Manel
Vallve, Maria de Lourdes Farre
Guil, Sonia
author_role author
author2 Castillo, Anaís Sánchez
Soler, Marta
Guardia, Aida Obiols
Piñeyro, David
Sastre, Raquel Boque
Cervantes, Maria E. Calleja
Moura, Manuel Castro de
Cardús, Anna Martínez
Rubio, Teresa
Pelletier, Joffrey
Iniesta, Maria Martínez
Martín, David Herrero
Tirado, Oscar M.
Gentilella, Antonio
Villanueva, Alberto
Esteller, Manel
Vallve, Maria de Lourdes Farre
Guil, Sonia
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Mateos, Cristina Oliveira
Castillo, Anaís Sánchez
Soler, Marta
Guardia, Aida Obiols
Piñeyro, David
Sastre, Raquel Boque
Cervantes, Maria E. Calleja
Moura, Manuel Castro de
Cardús, Anna Martínez
Rubio, Teresa
Pelletier, Joffrey
Iniesta, Maria Martínez
Martín, David Herrero
Tirado, Oscar M.
Gentilella, Antonio
Villanueva, Alberto
Esteller, Manel
Vallve, Maria de Lourdes Farre
Guil, Sonia
dc.subject.other.none.fl_str_mv Pseudogenes
Tumores
Proteína HMGA2
Prognóstico
topic Pseudogenes
Tumores
Proteína HMGA2
Prognóstico
Pseudogenes
Neoplasms
HMGA2 Protein
Prognosis
dc.subject.en.none.fl_str_mv Pseudogenes
Neoplasms
HMGA2 Protein
Prognosis
description Bellvitge Biomedical Research Institute. L’Hospitalet de Llobregat. Cancer Epigenetics and Biology Program. Barcelona, Catalonia, Spain.
publishDate 2019
dc.date.accessioned.fl_str_mv 2019-11-14T18:43:18Z
dc.date.available.fl_str_mv 2019-11-14T18:43:18Z
dc.date.issued.fl_str_mv 2019
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
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dc.identifier.citation.fl_str_mv MATEOS, Cristina Oliveira et al. The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition. Nature Communications, v. 10, p. 1-18, 2019.
dc.identifier.uri.fl_str_mv https://arca.fiocruz.br/handle/icict/37085
dc.identifier.issn.none.fl_str_mv 2041-1723
dc.identifier.doi.none.fl_str_mv 10.1038/s41467-019-11910-6
identifier_str_mv MATEOS, Cristina Oliveira et al. The transcribed pseudogene RPSAP52 enhances the oncofetal HMGA2-IGF2BP2-RAS axis through LIN28B-dependent and independent let-7 inhibition. Nature Communications, v. 10, p. 1-18, 2019.
2041-1723
10.1038/s41467-019-11910-6
url https://arca.fiocruz.br/handle/icict/37085
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