Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data in the presence of miR-29a inhibition in human dermal fibroblast cells

ABSTRACT: miR-29 can target many gene transcripts encoding extracellular matrix proteins. To unravel novel targets, we used microarray analysis to detect global gene expression changes when inhibiting endogenous miR-29. Total RNA from human dermal fibroblast cells after 48 h treatment with miR-29a inhibitor or control inhibitor were isolated and subjected to whole gene expression microarray analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Pei Zhang

PROVIDER: E-GEOD-45564 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

Ten-eleven translocation (Tet) and thymine DNA glycosylase (TDG), components of the demethylation pathway, are direct targets of miRNA-29a.

Zhang Pei P Huang Bihui B Xu Xiangru X Sessa William C WC

Biochemical and biophysical research communications 20130629 3

The ten-eleven translocation family of proteins (Tet1/2/3, Tets) converts 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), which can be further oxidized and repaired by thymine DNA glycosylase (TDG), to influence gene transcription in embryonic and adult tissues. However the mechanisms of how Tets and TDG levels are regulated are unknown. We show that miR-29 can directly regulate Tet1-3 and TDG mRNA levels through binding to their 3'UTRs. miR-29 mimic decreases global 5hmC levels, a hal ...[more]

PMID: 23820384

Similar Datasets

Project description:The miR-29 family is an important player in the molecular pathophysiology of distinct types of cancer, with roles that seems to depend on cellular context. Reduced miR-29 levels are associated with more aggressive disease and its overexpression in cancer and leukemic cell lines inhibits proliferation. In contrast, its overexpression in hematopoietic progenitors, promotes leukemogenesis. We explored the potential roles of miR-29a in the molecular pathophysiology of T-cell acute lymphoblastic leukemia (T-ALL). As compared to normal T-cells, miR-29a levels are extremely reduced in T-ALL and in the Jurkat cell line. Microarrays analysis in Jurkat cells, following the introduction of synthetic miR-29a mimics, revealed the down-regulation of several predicted targets, including previously described targets (DNMT3a/b, CDK6, PXDN, MCL1, PIK3R1 and CXXC6), and novel targets with roles in active DNA demethylation, such as members of the ten-eleven-translocation (TET) family and TDG. Reduced miR-29a levels contribute to altered epigenetics, as its introduction in Jurkat cells, promotes the demethylation of the AHR gene (commonly methylated in T-ALL). In T-ALL patients, miR-29a levels are significantly associated with blast counts and disease free survival. Our results highlight the relevance of miR-29 in T-ALL physiopathology, and may help to clarify some contrasting findings reported in the literature. In order to identify potential miR-29a targets in T-cell lymphoblastic leukemia, Jurkat cells were electroporated with synthetic RNA molecules corresponding to miR-29a mimics (pre-miR) or inhibitors (anti-miR); and microarray profiles were compared to the profiles of Jurkat cells eletroporated with the corresponding negative controls. Transcripts with levels reduced following the introduction of the pre-miR-29a (as compared to pre-miR-Control), or transcripts acumulated folowing introduction of the anti-miR-29a inhibitor (as compared to anti-miR-Control), were considered potential targets; and were further compared to microRNA target prediction databases. Two paired samples were used for this analysis.

Dataset Information

Expression data in the presence of miR-29a inhibition in human dermal fibroblast cells

Publications

Ten-eleven translocation (Tet) and thymine DNA glycosylase (TDG), components of the demethylation pathway, are direct targets of miRNA-29a.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure