Modulation of microRNA expression in human T-cell development: targeting of NOTCH3 by miR-150

Ghisi, Margherita; Corradin, Alberto; Basso, Katia; Frasson, Chiara; Serafin, Valentina; Mukherjee, Subhamoy; Mussolin, Lara; Ruggero, Katia; Bonanno, Laura; Guffanti, Alessandro; Bellis, Gianluca De; Gerosa, Gino; Stellin, Giovanni; D’Agostino, Donna M.; Basso, Giuseppe; Bronte, Vincenzo; Indraccolo, Stefano; Amadori, Alberto; Zanovello, Paola

doi:10.1182/blood-2010-12-326629

Cited by 204 publications

(188 citation statements)

References 50 publications

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“…In this study, we identified miR-150 as a new regulator for MLL-associated leukemia, one of the most aggressive leukemias with a poor prognosis. miR-150 is a key miRNA involved in hematopoiesis via suppression of Myb and other potential target genes (6,7,13,14,45,46). Altered expression of crucial developmental regulators is often linked with diseases and cancer transformation, so it was not surprising to observe that altered expression of miR-150 was detected in multiple hematopoietic disorders.…”

Section: Discussionmentioning

confidence: 99%

miR-150 Blocks MLL-AF9–Associated Leukemia through Oncogene Repression

Bousquet

Zhuang

et al. 2013

Molecular Cancer Research

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The microRNA miR-150, a critical regulator of hematopoiesis, is downregulated in mixed-lineage leukemia (MLL). In this study, miR-150 acts as a potent leukemic tumor suppressor by blocking the oncogenic properties of leukemic cells. By using MLL-AF9-transformed cells, we demonstrate that ectopic expression of miR-150 inhibits blast colony formation, cell growth, and increases apoptosis in vitro. More importantly, ectopic expression of miR-150 in MLL-AF9-transformed cells completely blocked the development of myeloid leukemia in transplanted mice. Furthermore, gene expression profiling revealed that miR-150 altered the expression levels of more than 30 "stem cell signature" genes and many others that are involved in critical cancer pathways. In addition to the known miR-150 target Myb, we also identified Cbl and Egr2 as bona fide targets and shRNA-mediated suppression of these genes recapitulated the pro-apoptotic effects observed in leukemic cells with miR-150 ectopic expression.In conclusion, we demonstrate that miR-150 is a potent leukemic tumor suppressor that regulates multiple oncogenes.Implications: These data establish new, key players for the development of therapeutic strategies to treat MLL-AF9-related leukemia. Mol Cancer Res; 11(8); 912-22. Ó2013 AACR.

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Section: Discussionmentioning

confidence: 99%

miR-150 Blocks MLL-AF9–Associated Leukemia through Oncogene Repression

Bousquet

Zhuang

et al. 2013

Molecular Cancer Research

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“…30 Since AA is a T cell mediated disease, it is interesting that miR-150-5p is selectively expressed in immature resting T cells and then strongly upregulated with their maturation and differentiation of the T-cell progresses. 28 MiR-150-5p is a circulating biomarker in female MG patients without immunosuppressive drug treatment, as the miR-150-5p level is reduced with clinical improvement after Circulating microRNA profile in aplastic anemia haematologica | 2017; 102 (1) 75 thymectomy. 21 Why miRNA expression changes is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…One of miR-150-5p targets is NOTCH3: the regulation of the Notch pathway through miR-150-5p may impact T-cell development. 28 Another target of miR-150-5p is the transcription factor C-MYB which plays an essential role in Tcell differentiation. 29 MiR-150-5p is an immuno-miRNA considered to be a crucial regulator of T-cell processes.…”

Section: Discussionmentioning

confidence: 99%

A plasma microRNA signature as a biomarker for acquired aplastic anemia

et al. 2016

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“…These immunomiRs play significant roles in Tcell development, maturation, activation, differentiation, and aging [70] . For example, miR150 [71] and miR181a [72] are involved in Tcell development, while miR21 [73] and miR1792 cluster [74,75] participate in Tcell activation.…”

Section: Mirnas and T-cell Regulationmentioning

confidence: 99%

miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

Zhang

2016

WJG

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Inflammatory bowel disease (IBD) is characterized by chronic relapsing inflammatory disorders of the gastrointestinal tract, and includes two major phenotypes: ulcerative colitis and Crohn's disease. The pathogenesis of IBD is not fully understood as of yet. It is believed that IBD results from complicated interactions between environmental factors, genetic predisposition, and immune disorders. miRNAs are a class of small non-coding RNAs that can regulate gene expression by targeting the 3′-untranslated region of specific mRNAs for degradation or translational inhibition. miRNAs are considered to play crucial regulatory roles in many biologic processes, such as immune cellular differentiation, proliferation, and apoptosis, and maintenance of immune homeostasis. Recently, aberrant expression of miRNAs was revealed to play an important role in autoimmune diseases, including IBD. In this review, we discuss the current understanding of how miRNAs regulate autoimmunity and inflammation by affecting the differentiation, maturation, and function of various immune cells. In particular, we focus on describing specific miRNA expression profiles in tissues and peripheral blood that may be associated with the pathogenesis of IBD. In addition, we summarize the opportunities for utilizing miRNAs as new biomarkers and as potential therapeutic targets in IBD.

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Modulation of microRNA expression in human T-cell development: targeting of NOTCH3 by miR-150

Abstract: Ontogenesis of T cells in the thymus is

Cited by 204 publications

References 50 publications

miR-150 Blocks MLL-AF9–Associated Leukemia through Oncogene Repression

miR-150 Blocks MLL-AF9–Associated Leukemia through Oncogene Repression

A plasma microRNA signature as a biomarker for acquired aplastic anemia

miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

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