miR-661 expression in SNAI1-induced epithelial to mesenchymal transition contributes to breast cancer cell invasion by targeting Nectin-1 and StarD10 messengers
| Autor: | Khalil Arar, Christina Laurini, Michèle Sabbah, Laurent Vallar, Michèle Moes, Charles-Henri Lecellier, Evelyne Friederich, A. Le Bechec, Guillaume Vetter, Anne Saumet, Charles Theillet |
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| Přispěvatelé: | Le Ster, Yves, Cytoskeleton and Cell Plasticity Lab, Université du Luxembourg (Uni.lu), Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), Université Montpellier 1 (UM1)-CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Centre de Recherche Publique- Santé, Centre de Recherche Saint-Antoine (UMRS893), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Sigma-Aldrich - Evry GENEPOLE, Sigma-Aldrich, Institut de Génétique Moléculaire de Montpellier (IGMM), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), This work was supported by grants from the Fond National de la Recherche (FNR) du Luxembourg, (BIOSAN), the Fondation Luxembourgeoise Contre le Cancer, Human Frontier Science Program (RGP0058/2005), INSERM and CNRS, France. A. Saumet is a recipient of a fellowship from the Ministère de la Culture, de l'Enseignement Supérieur et de la Recherche, Luxembourg (BFR 08/046). M. Moes and A. Le Béchec are supported by AFR grants from the Fond National de la Recherche, Luxembourg., CRLCC Val d'Aurelle - Paul Lamarque-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Université du Luxembourg ( Uni.lu ), Institut de recherche en cancérologie de Montpellier ( IRCM ), Université Montpellier 1 ( UM1 ) -CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université de Montpellier ( UM ), Centre de Recherche Saint-Antoine ( CR Saint-Antoine ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de Génétique Moléculaire de Montpellier ( IGMM ), Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ) |
| Rok vydání: | 2010 |
| Předmět: |
SNAI1
Cancer Research MESH : RNA Messenger MESH : Transcription Factors MESH : Cell Dedifferentiation Gene Expression MESH : Breast Neoplasms Biochemistry biophysics & molecular biology [F05] [Life sciences] Validation Studies as Topic MESH : RNA Small Interfering medicine.disease_cause Bioinformatics MESH : Neoplasm Invasiveness [ SDV.CAN ] Life Sciences [q-bio]/Cancer Metastasis 0302 clinical medicine MESH : Tumor Cells Cultured MESH : Validation Studies as Topic EMT/miR-661/ SNAI1/StarD10/Nectin-1/breast cancer cell invasion MESH: RNA Small Interfering Tumor Cells Cultured MESH : Female RNA Small Interfering Biochimie biophysique & biologie moléculaire [F05] [Sciences du vivant] Oligonucleotide Array Sequence Analysis 0303 health sciences EMT MESH: Transcription Factors MESH: Gene Expression Regulation Neoplastic MESH : Epithelial Cells Gene Expression Regulation Neoplastic MESH : Oligonucleotide Array Sequence Analysis MESH: Epithelial Cells 030220 oncology & carcinogenesis MESH: Cell Adhesion Molecules Female Breast disease StarD10 Nectin-1 MESH: Gene Expression MESH : Gene Expression Regulation Neoplastic Nectins Breast Neoplasms [SDV.CAN]Life Sciences [q-bio]/Cancer Biology MESH: Phosphoproteins MESH : Cell Adhesion Molecules MESH: Gene Expression Profiling 03 medical and health sciences [SDV.CAN] Life Sciences [q-bio]/Cancer microRNA Genetics medicine Humans Gene silencing Neoplasm Invasiveness RNA Messenger MESH: Tumor Cells Cultured Epithelial–mesenchymal transition Molecular Biology MESH: RNA Messenger 030304 developmental biology breast cancer cell invasion MESH: Validation Studies as Topic MESH: Humans MESH : Gene Expression Profiling Gene Expression Profiling MESH : Humans Cancer Epithelial Cells Mesenchymal Stem Cells MESH: Neoplasm Invasiveness Cell Dedifferentiation Phosphoproteins medicine.disease MESH: Cell Dedifferentiation miR-661 MESH : Gene Expression MESH : MicroRNAs MicroRNAs Retraction Note MESH: Mesenchymal Stem Cells MESH: Oligonucleotide Array Sequence Analysis Cancer research Snail Family Transcription Factors MESH : Phosphoproteins MESH : Mesenchymal Stem Cells Carcinogenesis Cell Adhesion Molecules MESH: MicroRNAs MESH: Female MESH: Breast Neoplasms Transcription Factors |
| Zdroj: | Oncogene Oncogene, 2010, 29 (31), pp.4436-48. ⟨10.1038/onc.2010.181⟩ Oncogene, Nature Publishing Group, 2010, 29 (31), pp.4436-48. ⟨10.1038/onc.2010.181⟩ Oncogene, 35(5), 670. Nature Publishing Group (2016). Oncogene, Nature Publishing Group, 2010, 29 (31), pp.4436-48. 〈10.1038/onc.2010.181〉 |
| ISSN: | 1476-5594 0950-9232 |
| Popis: | 4; International audience; Epithelial to mesenchymal transition (EMT) is a key step toward metastasis. MCF7 breast cancer cells conditionally expressing the EMT master regulator SNAI1 were used to identify early expressed microRNAs (miRNAs) and their targets that may contribute to the EMT process. Potential targets of miRNAs were identified by matching lists of in silico predicted targets and of inversely expressed mRNAs. MiRNAs were ranked based on the number of predicted hits, highlighting miR-661, a miRNA with so far no reported role in EMT. MiR-661 was found required for efficient invasion of breast cancer cells by destabilizing two of its predicted mRNA targets, the cell-cell adhesion protein Nectin-1 and the lipid transferase StarD10, resulting, in turn, in the downregulation of epithelial markers. Reexpression of Nectin-1 or StarD10 lacking the 3'-untranslated region counteracted SNAI1-induced invasion. Importantly, analysis of public transcriptomic data from a cohort of 295 well-characterized breast tumor specimen revealed that expression of StarD10 is highly associated with markers of luminal subtypes whereas its loss negatively correlated with the EMT-related, basal-like subtype. Collectively, our non-a priori approach revealed a nonpredicted link between SNAI1-triggered EMT and the down-regulation of Nectin-1 and StarD10 through the up-regulation of miR-661, which may contribute to the invasion of breast cancer cells and poor disease outcome. |
| Databáze: | OpenAIRE |
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