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miR-15a targets the HSP90 co-chaperone Morgana in chronic myeloid leukemia
Morgana is a ubiquitous HSP90 co-chaperone protein coded by the CHORDC1 gene. Morgana heterozygous mice develop with age a myeloid malignancy resembling human atypical myeloid leukemia (aCML), now renamed MDS/MPN with neutrophilia. Patients affected by this pathology exhibit low Morgana levels in th...
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| Published in: | Scientific reports 2024-07, Vol.14 (1), p.15089-11, Article 15089 |
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| creator | Poggio, Pietro Rocca, Stefania Fusella, Federica Ferretti, Roberta Ala, Ugo D’Anna, Flora Giugliano, Emilia Panuzzo, Cristina Fontana, Diletta Palumbo, Valeria Carrà, Giovanna Taverna, Daniela Gambacorti-Passerini, Carlo Saglio, Giuseppe Fava, Carmen Piazza, Rocco Morotti, Alessandro Orso, Francesca Brancaccio, Mara |
| description | Morgana is a ubiquitous HSP90 co-chaperone protein coded by the CHORDC1 gene. Morgana heterozygous mice develop with age a myeloid malignancy resembling human atypical myeloid leukemia (aCML), now renamed MDS/MPN with neutrophilia. Patients affected by this pathology exhibit low Morgana levels in the bone marrow (BM), suggesting that Morgana downregulation plays a causative role in the human malignancy. A decrease in Morgana expression levels is also evident in the BM of a subgroup of Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) patients showing resistance or an incomplete response to imatinib. Despite the relevance of these data, the mechanism through which Morgana expression is downregulated in patients’ bone marrow remains unclear. In this study, we investigated the possibility that Morgana expression is regulated by miRNAs and we demonstrated that Morgana is under the control of four miRNAs (miR-15a/b and miR-26a/b) and that miR-15a may account for Morgana downregulation in CML patients. |
| doi_str_mv | 10.1038/s41598-024-65404-7 |
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Morgana heterozygous mice develop with age a myeloid malignancy resembling human atypical myeloid leukemia (aCML), now renamed MDS/MPN with neutrophilia. Patients affected by this pathology exhibit low Morgana levels in the bone marrow (BM), suggesting that Morgana downregulation plays a causative role in the human malignancy. A decrease in Morgana expression levels is also evident in the BM of a subgroup of Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) patients showing resistance or an incomplete response to imatinib. Despite the relevance of these data, the mechanism through which Morgana expression is downregulated in patients’ bone marrow remains unclear. In this study, we investigated the possibility that Morgana expression is regulated by miRNAs and we demonstrated that Morgana is under the control of four miRNAs (miR-15a/b and miR-26a/b) and that miR-15a may account for Morgana downregulation in CML patients.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-024-65404-7</identifier><identifier>PMID: 38956394</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/337/384/331 ; 631/67/1990/283/1896 ; 631/80/470/1981 ; Animals ; Apoptosis ; Binding sites ; Bone marrow ; Bone Marrow - metabolism ; Bone Marrow - pathology ; Cancer ; Chronic myeloid leukemia ; Down-Regulation ; Gene Expression Regulation, Leukemic ; Genes ; Hematology ; HSP90 Heat-Shock Proteins - genetics ; HSP90 Heat-Shock Proteins - metabolism ; Hsp90 protein ; Humanities and Social Sciences ; Humans ; Imatinib ; Kinases ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology ; Malignancy ; Metastasis ; Mice ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Molecular Chaperones - genetics ; Molecular Chaperones - metabolism ; multidisciplinary ; Mutation ; Myelodysplastic syndrome ; Myeloid leukemia ; Neutrophilia ; Proteins ; Science ; Science (multidisciplinary) ; Stem cells ; Tumors</subject><ispartof>Scientific reports, 2024-07, Vol.14 (1), p.15089-11, Article 15089</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c422t-3bd003db87fcdfe6da9633e3e074927d9cff7d2dfbb01e7ae171796d7ba0dd9e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/3074884316/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3074884316?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38956394$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Poggio, Pietro</creatorcontrib><creatorcontrib>Rocca, Stefania</creatorcontrib><creatorcontrib>Fusella, Federica</creatorcontrib><creatorcontrib>Ferretti, Roberta</creatorcontrib><creatorcontrib>Ala, Ugo</creatorcontrib><creatorcontrib>D’Anna, Flora</creatorcontrib><creatorcontrib>Giugliano, Emilia</creatorcontrib><creatorcontrib>Panuzzo, Cristina</creatorcontrib><creatorcontrib>Fontana, Diletta</creatorcontrib><creatorcontrib>Palumbo, Valeria</creatorcontrib><creatorcontrib>Carrà, Giovanna</creatorcontrib><creatorcontrib>Taverna, Daniela</creatorcontrib><creatorcontrib>Gambacorti-Passerini, Carlo</creatorcontrib><creatorcontrib>Saglio, Giuseppe</creatorcontrib><creatorcontrib>Fava, Carmen</creatorcontrib><creatorcontrib>Piazza, Rocco</creatorcontrib><creatorcontrib>Morotti, Alessandro</creatorcontrib><creatorcontrib>Orso, Francesca</creatorcontrib><creatorcontrib>Brancaccio, Mara</creatorcontrib><title>miR-15a targets the HSP90 co-chaperone Morgana in chronic myeloid leukemia</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Morgana is a ubiquitous HSP90 co-chaperone protein coded by the CHORDC1 gene. Morgana heterozygous mice develop with age a myeloid malignancy resembling human atypical myeloid leukemia (aCML), now renamed MDS/MPN with neutrophilia. Patients affected by this pathology exhibit low Morgana levels in the bone marrow (BM), suggesting that Morgana downregulation plays a causative role in the human malignancy. A decrease in Morgana expression levels is also evident in the BM of a subgroup of Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) patients showing resistance or an incomplete response to imatinib. Despite the relevance of these data, the mechanism through which Morgana expression is downregulated in patients’ bone marrow remains unclear. 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Morgana heterozygous mice develop with age a myeloid malignancy resembling human atypical myeloid leukemia (aCML), now renamed MDS/MPN with neutrophilia. Patients affected by this pathology exhibit low Morgana levels in the bone marrow (BM), suggesting that Morgana downregulation plays a causative role in the human malignancy. A decrease in Morgana expression levels is also evident in the BM of a subgroup of Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) patients showing resistance or an incomplete response to imatinib. Despite the relevance of these data, the mechanism through which Morgana expression is downregulated in patients’ bone marrow remains unclear. 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| subjects | 631/337/384/331 631/67/1990/283/1896 631/80/470/1981 Animals Apoptosis Binding sites Bone marrow Bone Marrow - metabolism Bone Marrow - pathology Cancer Chronic myeloid leukemia Down-Regulation Gene Expression Regulation, Leukemic Genes Hematology HSP90 Heat-Shock Proteins - genetics HSP90 Heat-Shock Proteins - metabolism Hsp90 protein Humanities and Social Sciences Humans Imatinib Kinases Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Malignancy Metastasis Mice MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Molecular Chaperones - genetics Molecular Chaperones - metabolism multidisciplinary Mutation Myelodysplastic syndrome Myeloid leukemia Neutrophilia Proteins Science Science (multidisciplinary) Stem cells Tumors |
| title | miR-15a targets the HSP90 co-chaperone Morgana in chronic myeloid leukemia |
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