KIT signaling regulates MITF expression through miRNAs in normal and malignant mast cell proliferation

Lee, Youl Nam; Brandal, Stephanie; Noël, Pierre; Wentzel, Erik A.; Mendell, Joshua T.; McDevitt, Michael A.; Kapur, Reuben; Carter, Melody; Metcalfe, Dean D.; Takemoto, Clifford M.

doi:10.1182/blood-2010-07-293548

Cited by 58 publications

(59 citation statements)

References 33 publications

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“…In mast cells, CD117 (i.e. KIT or c-kit) represses miR-539 expression, thereby de-repressing microphthalmia-associated transcription factor expression and promoting proliferation (43). In other cell types, miR-539 expression may be biotin-sensitive, and miR-539 targets the mRNA of holocarboxylase synthase, which participates in genetic stability (44).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-539 Is Up-regulated in Failing Heart, and Suppresses O-GlcNAcase Expression

Muthusamy

DeMartino

Watson

et al. 2014

Journal of Biological Chemistry

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Background:Protein O-GlcNAcylation is nearly ubiquitous; however, regulation of the expression of key enzymes remains unknown. Results: miR-539 is up-regulated in the failing heart, binds to the 3ЈUTR, and negatively regulates O-GlcNAcase expression. Conclusion: Protein O-GlcNAcylation can be regulated by post-transcriptional mechanisms. Significance: miR-539 regulates one of the two enzymes responsible for O-GlcNAcylation in multicellular eukaryotes.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-539 Is Up-regulated in Failing Heart, and Suppresses O-GlcNAcase Expression

Muthusamy

DeMartino

Watson

et al. 2014

Journal of Biological Chemistry

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“…renal cell or esophageal carcinoma) [34,35]. miR-381 has been associated with neoplastic mast cell disorders due to its role in the regulatory cascade of stem-cell activity regulation [36]. Similar oncogenic or tumor-suppressive qualities have been described for the remaining microRNAs differentially expressed between NMZL and DLBCL, including the role of miR-422b as a regulatory element in DNA-mismatch-repair as well as the impact of miR-516-3p on metastatic activity [37].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Profiling of Low-Grade and Transformed Nodal Marginal Zone Lymphoma Reveals a Similar Signature Pattern Distinct from Diffuse Large B Cell Lymphoma

Gebauer

Thorns²,

Bernard³

et al. 2014

Acta Haematol

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Background/Aims: As critical post-transcriptional regulators of gene expression, microRNAs are involved in several cellular processes of vital impact including cell growth and apoptosis. Many hematologic malignancies exhibit distinct microRNA signatures. MicroRNA implication in the pathogenesis of nodal marginal zone lymphoma (NMZL), however, remains widely elusive. Methods: Comprehensive morphologic, immunophenotypic and cytogenetic studies were carried out on a cohort of NMZL (n = 30) incorporating indolent as well as transformed MZL. In addition, microRNA signatures were generated, employing a quantitative real-time polymerase chain reaction approach. These were then compared to signatures from cases of diffuse large B cell lymphoma (DLBCL) alongside reactive lymph node controls. Results: While microRNA signatures of low-grade and transformed NMZL did not differ significantly, several microRNAs were differentially expressed between transformed NMZL and DLBCL, hinting at molecularly distinct mechanisms of lymphomagenesis and indicating the biological disparity of transformed NMZL from DLBCL. Conclusion: In the light of the unresolved issue regarding the classification of marginal zone-derived transformed B-cell neoplasms, microRNAs may be a valuable aid in discriminating NMZL from DLBCL. © 2014 S. Karger AG, Basel

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“…In addition, miR-142-3p promotes FcεRI-mediated degranulation in mast cells [38]. With respect to the relationship between miRNAs and pathological conditions that are caused by malignant mast cell proliferation, Lee et al [53] reported that the miR-539 and miR-381 cluster was significantly down-regulated by c-Kit signaling, and the expression of these two miRNAs decreased Mitf protein levels and the colony-forming ability of mastocytosis cell lines. To determine the impact of the global depletion of miRNAs on mast cells, Oh et al [39] found that global miRNA expression was indispensable for murine mast cell development in vivo.…”

Section: The Mirna Target Gene Network Reflecting the Potential Mechamentioning

confidence: 99%

Altered MicroRNA Expression Profiles in Activated Mast Cells Following IgE-FcεRI Cross-Linking with Antigen

Teng¹,

Zhang²,

Yu³

et al. 2015

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs) are critical regulators of immune responses and immunologic disorders. However, little is known about miRNA expression and function during mast cell differentiation, proliferation and activation. This study aimed to determine the miRNA expression profiles in mast cells stimulated by immunoglobulin E (IgE) and antigen and to analyze the potential functions of specific miRNAs. Methods: Bone marrow-derived mast cells (BMMCs) generated from differentiated mouse bone marrow cells were untreated (Unstimu) or stimulated with IgE-antigen complexes for 1 h or 6 h (Stimu). The miRNA profiles were evaluated by miRNA microarray. MiRNA target gene prediction and enrichment analyses were performed using bioinformatics. Results: Seven significantly up-regulated and 10 down-regulated miRNAs were identified in the 1 h Stimu group relative to the Unstimu group (fold change>2; P<0.05). Of 8 miRNAs randomly selected from the 17 identified, the expression levels of 6 were confirmed by quantitative real-time PCR (qRT-PCR). The potential target genes of several candidate miRNAs were enriched in FcεRI signaling, response to stimulus and cellular exocytosis. Conclusion: The expression of many miRNAs changes following IgE-FcεRI cross-linking in activated mast cells, and these miRNAs probably play key regulatory roles in core signaling pathways and biological behaviors. Evaluating the functions of these characteristic miRNAs will further our understanding of IgE-associated allergic disease pathogenesis and the development of therapeutic strategies.

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KIT signaling regulates MITF expression through miRNAs in normal and malignant mast cell proliferation

Cited by 58 publications

References 33 publications

MicroRNA-539 Is Up-regulated in Failing Heart, and Suppresses O-GlcNAcase Expression

MicroRNA-539 Is Up-regulated in Failing Heart, and Suppresses O-GlcNAcase Expression

MicroRNA Profiling of Low-Grade and Transformed Nodal Marginal Zone Lymphoma Reveals a Similar Signature Pattern Distinct from Diffuse Large B Cell Lymphoma

Altered MicroRNA Expression Profiles in Activated Mast Cells Following IgE-FcεRI Cross-Linking with Antigen

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