A new molecular network comprising PU.1, interferon regulatory factor proteins and miR-342 stimulates ATRA-mediated granulocytic differentiation of acute promyelocytic leukemia cells

Marchis, Maria Laura De; Ballarino, Monica; Salvatori, Beatrice; Puzzolo, Maria-Cristina; Bozzoni, Irene; Fatica, Alessandro

doi:10.1038/leu.2008.372

Cited by 79 publications

(83 citation statements)

References 21 publications

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“…We showed that a set of miRs, including miR-100, 126, 126*, 181b, 181d, 223, and 342 were consistently up-regulated in CD34 ϩ EB cells, which indicates that these 7 miRs may represent a common feature of hematopoietic differentiation from hESCs. Among them, miRs-126/126*, 29,36 181b, 37 181d, 38 223 30,31 and 342 39 have a well-characterized association with the hematopoietic system and miRs-126/126* are the most highly up-regulated. miR-126 and 126* are processed from the same primary miR and located in an intron of Egfl7, a gene that is highly expressed in endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Regulated expression of microRNAs-126/126* inhibits erythropoiesis from human embryonic stem cells

Huang

Gschweng

Handel

et al. 2011

Blood

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IntroductionThe hematopoietic system is hierarchically organized, with a rare population of hematopoietic stem cells giving rise to specific progenitor cells and ultimately to diverse mature blood cell types. Lineage-specific fate decisions are intricately controlled by sets of master transcription factors. 1 For example, erythroid versus myeloid lineage differentiation is based on transcriptional crossantagonism between GATA-1 and PU.1. 2 PU.1 and C/EBP␣ are required for the generation of both macrophages and neutrophils. 3 In addition to transcription factors that are pivotal for hematopoietic cell lineage specification, several developmentally conserved signaling pathways, including Notch, Wnt, Sonic hedgehog, and TGF-␤, have also been implicated in regulating lineage determination. 4 MicroRNAs (miRs) are a recently discovered class of small (20-22 nt) noncoding RNAs that control gene expression posttranscriptionally by regulating mRNA translation or stability. 5 The roles of miRs in regulating the hematopoietic system are still poorly understood, although a series of recent studies have provided some perspective on this important issue. 6 There are several miRs, including miR-142, miR-181a, and miR-223, that are prominently expressed in hematopoietic cells. 7,8 Ectopic expression of miR-181a in hematopoietic stem/progenitor cells promotes B-cell differentiation, whereas overexpression of miR-142 and miR-223 leads to an increase in the proportion of T-lineage cells. 7 Some studies have not only delineated a role for miRs in hematopoiesis but also uncovered their molecular mechanisms of action involving regulation of lineage determining transcription factors. For example, the combination of gain-of-function and loss-of-function strategies has defined the requirement of miR-150 in B-cell differentiation by targeting the transcription factor c-Myb. 9 During monocytopoiesis, down-regulation of miRs 17-5p-20a-106a relieves the suppression of AML1, thus facilitating monocytic differentiation and maturation. 10 In addition to the role of specific miRs, the general requirement of miRs in hematopoiesis has been demonstrated, as deletion of Dicer in the thymus results in aberrant T-cell development in the murine system. 11,12 There is expanding literature suggesting that miRs also play an important role in the pathology of hematologic malignancies as tumor suppressor genes or oncogenes. For example, both miR-15a and miR-16 are deleted or down-regulated in the majority of chronic lymphocytic leukemia cases, 13 whereas C57BL6 mice transplanted with murine hematopoietic progenitor cells overexpressing miR-155 developed a myeloproliferative disorder. 14 Given compelling evidence that miRs are essential in the hematopoietic system, we sought to elucidate the potential roles of miRs in early human hematopoietic development. Insights into hematopoietic development have largely relied on findings from gene knockout and transgenic mouse models as well as in other model organisms. Because of the inaccessibility of human embryos,...

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Section: Discussionmentioning

confidence: 99%

Regulated expression of microRNAs-126/126* inhibits erythropoiesis from human embryonic stem cells

Huang

Gschweng

Handel

et al. 2011

Blood

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“…miR-107 has been shown to target the transcription factor NFI-A (Garzon et al, 2007), which participates with C/EBPa in the regulation of granulocyte differentiation-associated miR-223 expression (Fazi et al, 2005). miR-342 has been shown to stimulate granulocytic differentiation (De Marchis et al, 2009). Interestingly, the putative target of miR-342 MEIS1, a member of the TALE family of homeodomain Differentially expressed miRNAs in APL patients S Careccia et al genes, has been shown to have a pivotal role in normal hematopoiesis (Abramovich and Humphries, 2005;Diaz-Blanco et al, 2007) and it is frequently upregulated in human AMLs (Kumar et al, 2009).…”

Section: Differentially Expressed Mirnas In Apl Patientsmentioning

confidence: 99%

A restricted signature of miRNAs distinguishes APL blasts from normal promyelocytes

Careccia¹,

Mainardi

Pelosi³

et al. 2009

Oncogene

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MicroRNAs (miRNAs) are small non-coding RNAs involved in the regulation of critical cell processes such as apoptosis, cell proliferation and differentiation. A small set of miRNAs is differentially expressed in hematopoietic cells and seemingly has an important role in granulopoiesis and lineage differentiation. In this study, we analysed, using a quantitative real-time PCR approach, the expression of 12 granulocytic differentiation signature miRNAs in a cohort of acute promyelocytic leukemia (APL) patients. We found nine miRNAs overexpressed and three miRNAs (miR-107, -342 and let-7c) downregulated in APL blasts as compared with normal promyelocytes differentiated in vitro from CD34 þ progenitors. Patients successfully treated with all-trans-retinoic acid (ATRA) and chemotherapy showed downregulation of miR-181b and upregulation of miR-15b, -16, -107, -223, -342 and let-7c. We further investigated whether the APL-associated oncogene, promyelocytic leukemia gene (PML)/retinoic acid receptor a (RARa), might be involved in the transcriptional repression of miR-107, -342 and let-7c. We found that PML/RARa binds the regulatory sequences of the intragenic miR-342 and let-7c. In addition, we observed, in response to ATRA, the release of PML/ RARa paralleled by their transcriptional activation, together with their host genes, EVL and C21orf34a. In conclusion, we show that a small subset of miRNAs is differentially expressed in APL and modulated by ATRA-based treatment.

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“…These findings are supported by the fact that IRF-1 Ϫ/Ϫ mice have defective myelopoiesis, which is partly caused by down-regulation of PU.1, 42 and that infection of neutrophil precursors with Anaplasma phagocytophilum results in down-regulation of both IRF-1 and PU.1. 43 A cooperative function between IRF-1 and PU.1 has been reported during all-trans retinoic acid-mediated granulopoiesis 44 and in IFN-␥-stimulated myeloid cells. 45 Furthermore, IRF-1 is naturally down-regulated toward the final stages of erythroid maturation, 46 which overall sustains the notion that suppression of the IRF-1-PU.1 axis is a prerequisite for normal erythropoiesis.…”

Section: Impact Of Ifn-␥ On the Erythroid Balance 2585mentioning

confidence: 99%

Chronic IFN-γ production in mice induces anemia by reducing erythrocyte life span and inhibiting erythropoiesis through an IRF-1/PU.1 axis

Libregts

Gutiérrez²,

Bruin

et al. 2011

Blood

181

157

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A new molecular network comprising PU.1, interferon regulatory factor proteins and miR-342 stimulates ATRA-mediated granulocytic differentiation of acute promyelocytic leukemia cells

Cited by 79 publications

References 21 publications

Regulated expression of microRNAs-126/126* inhibits erythropoiesis from human embryonic stem cells

Regulated expression of microRNAs-126/126* inhibits erythropoiesis from human embryonic stem cells

A restricted signature of miRNAs distinguishes APL blasts from normal promyelocytes

Chronic IFN-γ production in mice induces anemia by reducing erythrocyte life span and inhibiting erythropoiesis through an IRF-1/PU.1 axis

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