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An antisense transcript mediates MALAT1 response in human breast cancer

BACKGROUND: Long non-coding RNAs (lncRNAs) represent a substantial portion of the human transcriptome. LncRNAs present a very stringent cell-type/tissue specificity being potential candidates for therapeutical applications during aging and disease. As example, targeting of MALAT1, a highly conserved...

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Autores principales: Gomes, Carla Pereira, Nóbrega-Pereira, Sandrina, Domingues-Silva, Beatriz, Rebelo, Kenny, Alves-Vale, Catarina, Marinho, Sérgio Pires, Carvalho, Tânia, Dias, Sérgio, Bernardes de Jesus, Bruno
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683341/
https://www.ncbi.nlm.nih.gov/pubmed/31382922
http://dx.doi.org/10.1186/s12885-019-5962-0
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author Gomes, Carla Pereira
Nóbrega-Pereira, Sandrina
Domingues-Silva, Beatriz
Rebelo, Kenny
Alves-Vale, Catarina
Marinho, Sérgio Pires
Carvalho, Tânia
Dias, Sérgio
Bernardes de Jesus, Bruno
author_facet Gomes, Carla Pereira
Nóbrega-Pereira, Sandrina
Domingues-Silva, Beatriz
Rebelo, Kenny
Alves-Vale, Catarina
Marinho, Sérgio Pires
Carvalho, Tânia
Dias, Sérgio
Bernardes de Jesus, Bruno
author_sort Gomes, Carla Pereira
collection PubMed
description BACKGROUND: Long non-coding RNAs (lncRNAs) represent a substantial portion of the human transcriptome. LncRNAs present a very stringent cell-type/tissue specificity being potential candidates for therapeutical applications during aging and disease. As example, targeting of MALAT1, a highly conserved lncRNA originally identified in metastatic non-small cell lung cancer, has shown promising results in cancer regression. Nevertheless, the regulation and specificity of MALAT1 have not been directly addressed. Interestingly, MALAT1 locus is spanned by an antisense transcript named TALAM1. METHODS: Here using a collection of breast cancer cells and in vitro and in vivo migration assays we characterized the dynamics of expression and demonstrated that TALAM1 regulates and synergizes with MALAT1 during tumorigenesis. RESULTS: Down-regulation of TALAM1 was shown to greatly impact on the capacity of breast cancer cells to migrate in vitro or to populate the lungs of immunocompromised mice. Additionally, we demonstrated that TALAM1 cooperates with MALAT1 in the regulation of the properties guiding breast cancer aggressiveness and malignancy. CONCLUSIONS: By characterizing this sense/anti-sense pair we uncovered the complexity of MALAT1 locus regulation, describing new potential candidates for cancer targeting. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12885-019-5962-0) contains supplementary material, which is available to authorized users.
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spelling pubmed-66833412019-08-09 An antisense transcript mediates MALAT1 response in human breast cancer Gomes, Carla Pereira Nóbrega-Pereira, Sandrina Domingues-Silva, Beatriz Rebelo, Kenny Alves-Vale, Catarina Marinho, Sérgio Pires Carvalho, Tânia Dias, Sérgio Bernardes de Jesus, Bruno BMC Cancer Research Article BACKGROUND: Long non-coding RNAs (lncRNAs) represent a substantial portion of the human transcriptome. LncRNAs present a very stringent cell-type/tissue specificity being potential candidates for therapeutical applications during aging and disease. As example, targeting of MALAT1, a highly conserved lncRNA originally identified in metastatic non-small cell lung cancer, has shown promising results in cancer regression. Nevertheless, the regulation and specificity of MALAT1 have not been directly addressed. Interestingly, MALAT1 locus is spanned by an antisense transcript named TALAM1. METHODS: Here using a collection of breast cancer cells and in vitro and in vivo migration assays we characterized the dynamics of expression and demonstrated that TALAM1 regulates and synergizes with MALAT1 during tumorigenesis. RESULTS: Down-regulation of TALAM1 was shown to greatly impact on the capacity of breast cancer cells to migrate in vitro or to populate the lungs of immunocompromised mice. Additionally, we demonstrated that TALAM1 cooperates with MALAT1 in the regulation of the properties guiding breast cancer aggressiveness and malignancy. CONCLUSIONS: By characterizing this sense/anti-sense pair we uncovered the complexity of MALAT1 locus regulation, describing new potential candidates for cancer targeting. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12885-019-5962-0) contains supplementary material, which is available to authorized users. BioMed Central 2019-08-05 /pmc/articles/PMC6683341/ /pubmed/31382922 http://dx.doi.org/10.1186/s12885-019-5962-0 Text en © The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Gomes, Carla Pereira
Nóbrega-Pereira, Sandrina
Domingues-Silva, Beatriz
Rebelo, Kenny
Alves-Vale, Catarina
Marinho, Sérgio Pires
Carvalho, Tânia
Dias, Sérgio
Bernardes de Jesus, Bruno
An antisense transcript mediates MALAT1 response in human breast cancer
title An antisense transcript mediates MALAT1 response in human breast cancer
title_full An antisense transcript mediates MALAT1 response in human breast cancer
title_fullStr An antisense transcript mediates MALAT1 response in human breast cancer
title_full_unstemmed An antisense transcript mediates MALAT1 response in human breast cancer
title_short An antisense transcript mediates MALAT1 response in human breast cancer
title_sort antisense transcript mediates malat1 response in human breast cancer
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683341/
https://www.ncbi.nlm.nih.gov/pubmed/31382922
http://dx.doi.org/10.1186/s12885-019-5962-0
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