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MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2 [mRNA]

ABSTRACT: We analyzed mK562 cells with miR-543 overexpressed or empty vector to determine the mRNA profile of miR-543 overexpressed K562 cells. We used Affymetrix Clariom S Human Array to profile the differentially expressed mRNA in miR-543 overexpressed and control cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE142236 | GEO | 2019/12/18

REPOSITORIES: GEO

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miR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2.

Project description:Myelofibrosis (MF) is a myeloproliferative neoplasm characterized by cytopenia and extramedullary hematopoiesis, resulting in splenomegaly. Multiple pathological mechanisms (e.g., circulating cytokines and genetic alterations, such as JAKV617F mutation) have been implicated in the etiology of MF, but the molecular mechanism causing resistance to JAK2V617F inhibitor therapy remains unknown. Among MF patients who were treated with the JAK inhibitor ruxolitinib, we compared noncoding RNA profiles of ruxolitinib therapy responders versus nonresponders and found miR-543 was significantly upregulated in nonresponders. We validated these findings by reverse transcription-quantitative PCR. in this same cohort, in 2 additional independent MF patient cohorts from the United States and Romania, and in a JAK2V617F mouse model of MF. Both in vitro and in vivo models were used to determine the underlying molecular mechanism of miR-543 in MF. Here, we demonstrate that miR-543 targets the dioxygenases ten-eleven translocation 1 (TET1) and 2 (TET2) in patients and in vitro, causing increased levels of global 5-methylcytosine, while decreasing the acetylation of histone 3, STAT3, and tumor protein p53. Mechanistically, we found that activation of STAT3 by JAKs epigenetically controls miR-543 expression via binding the promoter region of miR-543. Furthermore, miR-543 upregulation promotes the expression of genes related to drug metabolism, including CYP3A4, which is involved in ruxolitinib metabolism. Our findings suggest miR-543 as a potentially novel biomarker for the prognosis of MF patients with a high risk of treatment resistance and as a potentially new target for the development of new treatment options.

| S-EPMC7030823 | biostudies-literature

MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2 [mRNA]

Project description:MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2 [mRNA]

| PRJNA596275 | ENA

MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2

Project description:MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2

| PRJNA596276 | ENA

MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2 [miRNA]

Project description:MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2 [miRNA]

| PRJNA596272 | ENA

MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2 [miRNA]

Project description:We analyzed 14 patients with Myelofibrosis (MF) to determine the miRNA profile of patients not responding to current MF treatment. We used Affymetrix miRNA-3 array to profile the differentially expressed miRNA in bone-marrow between patients with MF that respond to current MF treatment and the patients with MF that do not respond to current MF treatment.

2019-12-18 | GSE142239 | GEO

MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-12-18 | GSE142240 | GEO

Sinorhizobium medicae strain:543

Project description:Sinorhizobium medicae 543 Resequencing

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Tet1 and Tet2 Protect DNA Methylation Canyons against Hypermethylation.

Project description:DNA methylation is a dynamic epigenetic modification with an important role in cell fate specification and reprogramming. The Ten eleven translocation (Tet) family of enzymes converts 5-methylcytosine to 5-hydroxymethylcytosine, which promotes passive DNA demethylation and functions as an intermediate in an active DNA demethylation process. Tet1/Tet2 double-knockout mice are characterized by developmental defects and epigenetic instability, suggesting a requirement for Tet-mediated DNA demethylation for the proper regulation of gene expression during differentiation. Here, we used whole-genome bisulfite and transcriptome sequencing to characterize the underlying mechanisms. Our results uncover the hypermethylation of DNA methylation canyons as the genomic key feature of Tet1/Tet2 double-knockout mouse embryonic fibroblasts. Canyon hypermethylation coincided with disturbed regulation of associated genes, suggesting a mechanistic explanation for the observed Tet-dependent differentiation defects. Based on these results, we propose an important regulatory role of Tet-dependent DNA demethylation for the maintenance of DNA methylation canyons, which prevents invasive DNA methylation and allows functional regulation of canyon-associated genes.

| S-EPMC4719427 | biostudies-literature

Colletotrichum trifolii strain:543-2

Project description:Colletotrichum trifolii strain:543-2 Genome sequencing and assembly

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Screening for potential target genes of hsa-mir-199a-1 and hsa-mir-4423 using Clariom D arrays

Project description:We screened for target genes of hsa-mir-199a-1 and hsa-mir-4423 by transcriptome profiling. The miRNAs were overexpressed in HeLa cells by transient transfection of precursor miRNA expression plasmids. High-density Clariom D arrays for human were used for the gene expression analysis. This GEO entry provides the microarray data preprocessed according to the gene level workflow.

2021-10-15 | GSE185859 | GEO

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