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Inactivation of TP53 correlates with disease progression and low miR-34a expression in previously treated chronic lymphocytic leukemia patients

ABSTRACT: Micro-RNA expression data of CD19 selected B-cells from previously treated and relapsed chronic lymphocytic leukemia patients. We aimed to correlate miR-34a with TP53 mutation status and del17p status.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45328 | GEO | 2013/03/21

SECONDARY ACCESSION(S): PRJNA193479

REPOSITORIES: GEO

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Inactivation of TP53 correlates with disease progression and low miR-34a expression in previously treated chronic lymphocytic leukemia patients

Project description:Micro-RNA expression data of CD19 selected B-cells from previously treated and relapsed chronic lymphocytic leukemia patients. We aimed to correlate miR-34a with TP53 mutation status and del17p status. CD19 B-cells from previously treated and relapsed chronic lymphocytic leukemia patients were selected for RNA extraction and hybridization on Affymetrix microarrays.

2013-03-21 | E-GEOD-45328 | biostudies-arrayexpress

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2019-10-14 | PXD015278 | Pride

Pisolithus sp. 34A

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Project description:Analysis NCI-H1299 lung cancer cells transfected with synthetic oligo mimics for microRNAs (miRNAs) miR-34a and ghR-34a. We developed a 30-nucleotide single-strand RNA (ssRNA), termed “guide hairpin RNA (ghR),” that has a physiological function similar to that of miRNA and siRNA. The ghR caused no innate cytokine response either in vitro or in vivo. In addition, its structure does not contain a passenger strand seed sequence, reducing the potential for off-target effects relative to existing short RNA reagents. Systemic injection of ghR-form miR-34a (ghR-34a) suppressed tumor growth in a mouse model of RAS-induced lung cancer. Furthermore, ghR-34a functioned in a Dicer- and Ago2-independent manner. This novel RNAi technology may provide a novel, safe, and effective nucleic acid drug platform that will increase the clinical usefulness of nucleic acid therapy. MiR-34a–targeted mRNAs regulated by mRNA degradation rather than translational inhibition were identified using microarray data from miR-34 and ghR-34a transfectants.

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NCI-H1299 lung cancer cell line transfected with miR-34a and ghR-34a

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Project description:To investigate the behavior of RNA Pol II during RNA activation by miR-34a,the ChIP-Seq analysis of RNA Poll II in NCI-H1299 cell line was performed. This experiment analyzes how RNA pol II is activated by the introduction of miR-34a in some genes whose transcription is induced by miR-34a. From the analysis of this data, the purpose is to clarify the molecular mechanism of RNA activation by miR-34a.

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Gene expression profile (GEP) of miR-34a-5p-overexpressing CD34+ HPCs

Project description:Primary Myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by hyperplastic megakaryopoiesis and myelofibrosis. Through a gene expression profile (GEP) study we recently highlighted the upregulationof miR-34a-5p in PMF versus healthy donor (HD) CD34+ hematopoietic progenitor cells (HPCs). To shed some light into the role of miR-34a-5p in PMF pathogenesis, here we unravelled the effects of the overexpression of miR-34a-5p in HPCs forcing its expression in HPCs. We showed that enforced expression of miR-34a-5p blocks proliferation and favours the megakaryocyte and monocyte/macrophage commitment of HPCs. Interestingly, we identified lymphoid enhancer-binding factor 1 (LEF1) and nuclear receptor subfamily 4, group A, member 2 (NR4A2) transcripts as miR-34a-5p-targets downregulated after miR-34a-5p overexpression in HPCs as well as in PMF compared with HD HPCs. Remarkably, the knockdown of NR4A2 in HPCs mimicked the antiproliferative effects of miR-34a-5p overexpression, while the silencing of LEF1 phenocopied the effects of miR-34a-5p overexpression in HPCs lineage choice, by stimulating the megakaryocyte and monocyte/macrophage commitment.

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