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The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans

ABSTRACT: We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE16050 | GEO | 2010/03/22

SECONDARY ACCESSION(S): PRJNA114993

REPOSITORIES: GEO

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Project description:Increasing evidences support a potential role for the Signal Transducer and Activator of Transcription-3 (STAT3) as a tumor driver in cutaneous T-cell lymphoma (CTCL). However, the mechanisms leading to STAT3 pathway activation in CTCL and how STAT3 activation contributes to lymphomagenesis remains primarily not enough explored. Recently, we found that miR-124, a known STAT3 regulator in cancer, is robustly silenced in Mycosis Fungoides (MF) tumor-stage and CTCL cell lines and we have herein studied whether deregulation of miR-124 contributes to activate STAT3 pathway in CTCL. Material and Methods: DNA methylation status of miR-124 and its expression levels in response to the DNA-demethylating agent azacitidine were evaluated in CTCL cell lines by pyrosequencing analysis. CTCL cell lines were transient transfected with a lentiviral vector encoding miR-124 and transfected cells were analyzed for phosphorylated STAT3 (P-STAT3) levels. The impact on STAT3 signaling was evaluated using expression microarray on CTCL cell lines in both conditions, miR-124 absent (malignant condition) versus miR-124 expressed (lentiviral transduction). Results: A significant promoter methylation and silencing of miR-124 in MF tumor samples and CTCL cell lines was detected. DNA methylation levels of miR-124 in CTCL cell lines were restored (and subsequently miR-124 were overexpressed) after DNA demethylation. Ectopic lentiviral expression of miR-124 downregulated STAT3 in the different CTCL cell lines. Genes differentially expressed regarding miR-124 regulation in CTCL cell lines indicated impact on known cell survival and function pathways and, particularly, intervention on miR-124 expression modulated different STAT3 pathway components. Conclusions: Our study deciphers a novel epigenetic mechanisms regulating STAT3 pathway in CTCL. This might contribute to a better understanding the molecular basis in CTCL development. Deregulation of STAT3 seems to have a major impact on cell survival in CTCL cell lines indicating the potential interest of targeting STAT3 with specific therapies.

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The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans

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