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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71423 | GEO | 2015/07/29

SECONDARY ACCESSION(S): PRJNA291182

REPOSITORIES: GEO

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

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.

2015-07-29 | E-GEOD-71423 | biostudies-arrayexpress

Identification of SART3 as a pre-miR-34a–binding protein

Project description:MicroRNAs (miRNAs or miRs) are small, noncoding RNAs that are implicated in the regulation of nearly all biological processes. Global miRNA biogenesis is altered in many cancers and RNA-binding proteins (RBPs) have been shown to play a role in this process, presenting a promising avenue for targeting miRNA dysregulation in disease. miR-34a exhibits tumor-suppressive functions by targeting cell cycle regulators CDK4/6 and anti-apoptotic factor Bcl-2, among other regulatory pathways such as Wnt, TGF-, and Notch signaling. Many cancers show downregulation or loss of miR-34a, and synthetic miR-34a supplementation has been shown to inhibit tumor growth in vivo; however, the post-transcriptional mechanisms by which miR-34a is lost in cancer are not entirely understood. Here, we have used a proteomics-mediated approach to identify Squamous cell carcinoma antigen recognized by T-cells 3 (SART3) as a putative pre-miR-34a-binding protein. SART3 is a spliceosome recycling factor and nuclear RBP with no previously reported role in miRNA regulation. We demonstrate that SART3 binds pre-miR-34a with specificity over pre-let-7d and begin to elucidate a new functional role for this protein in non-small lung cancer cells. Overexpression of SART3 led to increased miR-34a levels, downregulation of the miR-34a target genes CDK4 and CDK6, and cell cycle arrest in the G1 phase. In vitro binding studies showed that the RNA-recognition motifs within the SART3 sequence are responsible for selective pre-miR-34a binding. Collectively, our results present evidence for an influential role of SART3 in miR-34a biogenesis and cell cycle progression.

2019-10-14 | PXD015278 | Pride

RNA-seq of mimic miR-34a transfected H1299 and DDX21 KO cell lines.

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Transcriptional profiling of lung cancer cells over-expression miR-34a.

Project description:The Zeb1 transcriptional repressor plays a key role in metastasis through the down-regulation of genes that are strong inducers of epithelial differentiation and inhibitors of stem-ness. Here we report that Zeb1 controls the expression of numerous oncogenic and tumor suppressive microRNAs (miRs). Zeb1 stimulated pro-migratory cytoskeletal processes by down-regulating miR-34a and activated Rho GTPases through Arhgap1, a Cdc42 GTPase activating protein and novel miR-34a target gene. Poor-prognosis human lung adenocarcinomas were highly enriched in a cytoskeletal gene signature activated by miR-34a down-regulation. These findings suggest that Zeb1 regulates a miR network and drives pro-migratory cytoskeletal processes through miR-34a.

2012-08-09 | GSE38341 | GEO

Transcriptional profiling of lung cancer cells over-expression miR-34a.

2012-08-08 | E-GEOD-38341 | biostudies-arrayexpress

Homo sapiens

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

| PRJNA291182 | ENA

Identification of human miR-34a-responsive transcripts

Project description:In order to examine the consequences of human miR-34a induction on the transcriptome, HCT116 cells (a colon cancer cell line) were infected with a retrovirus that produces miR-34a. Gene expression profiles were then monitored using Affymetrix microarrays. Affymetrix microarrays were used to examine the transcriptomes of HCT116 cells infected with an empty retroviral vector (pMSCV-PIG) or a retroviral vector that expresses human miR-34a. Keywords: comparison of cells with or without enforced miR-34a expression

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Poll II ChIP-Seq in miR-34a transfectant

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.

2021-02-01 | GSE161321 | GEO

Understanding downstream signaling pathways regulated by miR-34a-5p in articular cartilage by RNA sequencing using miR-34a knock-out mice

Project description:The goal of this study was to determine the role of miR-34a in regulating chondrocyte transcript profiles. Next Generation Sequencing of total RNA extracted from mouse KO and WT chondrocytes revealed 175 significantly differentially expressed genes (84 up, 91 down) in miR-34a KO chondrocytes compared to WT cells. We are currently validating potential direct targets of miR-34a from our NGS data and performing computational pathway analysis to identify novel pathways regulated by miR-34a.

2021-03-08 | GSE133775 | GEO

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.

2017-03-08 | GSE89156 | GEO

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