MiR-378a-3p is critical for Burkitt lymphoma cell growth
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA594376 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To gain further knowledge on the role of microRNAs (miRNAs) in the pathogenesis of Burkitt lymphoma (BL), we performed small RNA sequencing in BL cell lines and normal germinal center B (GC-B) cells. This revealed 26 miRNAs with significantly different expression levels. Altered levels were validated by qRT-PCR for six of eight selected miRNAs. For five miRNAs, the differential expression pattern was confirmed in BL primary tissues compared to GC-B cells. Inhibition of miR-378a-3p reduced the growth of multiple BL cell lines. RNA immunoprecipitation of Argonaute 2 followed by microarray analysis (Ago2-RIP-Chip) upon inhibition and ectopic overexpression of miR-378a-3p revealed 63 and 20 putative miR-378a-3p targets, respectively. These included 28 genes with a putative miR-378a-3p binding site. Effective targeting by miR-378a-3p was confirmed by luciferase reporter assays for four out of eight selected genes: MNT, FOXP1, IRAK4, and lncRNA JPX, all of which have been implicated in proliferation and cancer. In summary, our study identified several differentially expressed miRNAs in BL. We identified miR-378a-3p as a miRNA with an oncogenic role in BL and revealed 4 novel miR-378a-3p target genes, i.e. MNT, FOXP1, IRAK4, and JPX.
2020-06-30 | GSE141691 | GEO
Project description:Wild-type (WT) miR-378a-3p or edited miR-378a-3p were expressed in SB2 KD-ADAR1 cells to identify the genes regulated by edited miR-378a-3p vs WT miR-378a-3p. PARVA was one of the genes identified to be regulated by edited miR-378a-3p. We demonstrate that this regulation of PARVA is lost in highly metastatic melanoma cells. Microarray analysis was used to evaluate the robustness and reproducibility of the method used to generate the ex vivo tumor tissue model and confirm its ability to recapitulate the essential features of the original tumor.
2018-02-22 | GSE107088 | GEO
Project description:MicroRNAs (miRNAs) are small RNA molecules with important gene regulatory roles in normal and pathophysiological cellular processes. Burkitt lymphoma (BL) is an MYC-driven lymphoma of germinal center B (GC-B) cell origin. To gain further knowledge on the role of miRNAs in the pathogenesis of BL, we performed small RNA sequencing in BL cell lines and normal GC-B cells. This revealed 26 miRNAs with significantly different expression levels. For five miRNAs, the differential expression pattern was confirmed in primary BL tissues compared to GC-B cells. MiR-378a-3p was upregulated in BL, and its inhibition reduced the growth of multiple BL cell lines. RNA immunoprecipitation of Argonaute 2 followed by microarray analysis (Ago2-RIP-Chip) upon inhibition and ectopic overexpression of miR-378a-3p revealed 63 and 20 putative miR-378a-3p targets, respectively. Effective targeting by miR-378a-3p was confirmed by luciferase reporter assays for MAX Network Transcriptional Repressor (MNT), Forkhead Box P1 (FOXP1), Interleukin 1 Receptor Associated Kinase 4 (IRAK4), and lncRNA Just Proximal To XIST (JPX), and by Western blot for IRAK4 and MNT. Overexpression of IRAK4 and MNT phenocopied the effect of miR-378a-3p inhibition. In summary, we identified miR-378a-3p as a miRNA with an oncogenic role in BL and identified IRAK4 and MNT as miR-378a-3p target genes that are involved in its growth regulatory role.
| S-EPMC7760147 | biostudies-literature
Project description:Epstein-Barr virus is associated with several human malignancies, including Burkitt Lymnphoma. The virus encodes more than 40 microRNAs, which participate in its possible pathogenetic role. We used microarrays to study the effect of the expression of an Epstein-Barr virus-encoded microRNA (ebv-BART6-3p) on the global gene expression profile of Burkitt Lymphoma cell lines.
2016-03-02 | GSE63665 | GEO
Project description:Edited miR-378a-3p target genes
| PRJNA418978 | ENA
Project description:Burkitt lymphoma is the commonest cancer in children in Africa. We compared the gene expression profiles of African Burkitt lymphoma patients with those of cases presented in Western countries in both immunocompetent (sporadic Burkitt lymphoma) and HIV-infected patients (immunodeficiency associated Burkitt lymphoma). We used microarrays to detail the global programme of gene expression in different subtypes of Burkitt lymphoma.
2011-01-20 | GSE26673 | GEO
Project description:Burkitt lymphoma is the commonest cancer in children in Africa. We compared the gene expression profiles of African Burkitt lymphoma patients with those of cases presented in Western countries in both immunocompetent (sporadic Burkitt lymphoma) and HIV-infected patients (immunodeficiency associated Burkitt lymphoma). We used microarrays to detail the global programme of gene expression in different subtypes of Burkitt lymphoma. Lymph-node biopsies were collected at diagnosis. Gene expression profiles were generated with the Affymetrix HG U133 2.0 plus microarray
2011-01-20 | E-GEOD-26673 | biostudies-arrayexpress
Project description:Epstein-Barr virus is associated with several human malignancies, including Burkitt Lymnphoma. The virus encodes more than 40 microRNAs, which participate in its possible pathogenetic role. We used microarrays to study the effect of the expression of an Epstein-Barr virus-encoded microRNA (ebv-BART6-3p) on the global gene expression profile of Burkitt Lymphoma cell lines. In order to determine the BART6-3p targets, EBV-negative Akata 2A8 or EBV-positive Akata cells were transiently transfected (in duplicates) with synthetic BART6-3p mimic or inhibitor (100 nM; Custom synthesized by Dharmacon- Thermo Scientific, Germany), respectively. For each treatment, a further transfection with corresponding negative control was performed as well (10 nM; I-300145-01, Dharmacon- Thermo Scientific, Germany). The transfection of 5,000,000 cells per treatment was performed by Amaxa nucleofector apparatus (Amaxa, Cologne-Germany), using the program G23 and the transfection solution V according to the manufacturerâs instructions. Transfection efficiency was assessed by means of a further treatment (2µg of pmaxGFP) and detection of both fluorescence and cell viability by flow cytometry. Twenty four hours post-transfection, cells were harvested and RNA was extracted using Trizol, and transfection efficiency was further confirmed by evaluating the expression level of BART6-3p using q-PCR by means of Taqman probes, employing RNU43 as housekeeping miRNA (Applied Biosystems, Cologne, Germany). RNA was further hybridized to HuGene-2.0-st array (Affymetrix, Santa Clara, CA) according to the manufacturer's instructions.
2016-03-02 | E-GEOD-63665 | biostudies-arrayexpress
Project description:Burkitt Lymphoma patient samples using gene expression to create a molecular definition of the disease. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Keywords: clinical history design Samples were obtained from patients with Burkitt lymphoma and gene expression profiling was used to create a molecular definition of the disease. The molecular definition was then used to predict the disease in an independent set of patients with atypical Burkitt lymphoma and diffuse large B cell lymphoma.
2006-07-04 | E-GEOD-4732 | biostudies-arrayexpress
Project description:Burkitt lymphoma is characterized by deregulation of MYC, but the contribution of other genetic mutations to the disease is largely unknown. Here, we describe the first completely sequenced genome from a Burkitt lymphoma tumor and germline DNA from the same affected individual. We further sequenced the exomes of 59 Burkitt lymphoma tumors and compared them to sequenced exomes from 94 diffuse large B-cell lymphoma (DLBCL) tumors. We identified 70 genes that were recurrently mutated in Burkitt lymphomas, including ID3, GNA13, RET, PIK3R1 and the SWI/SNF genes ARID1A and SMARCA4. Our data implicate a number of genes in cancer for the first time, including CCT6B, SALL3, FTCD and PC. ID3 mutations occurred in 34% of Burkitt lymphomas and not in DLBCLs. We show experimentally that ID3 mutations promote cell cycle progression and proliferation. Our work thus elucidates commonly occurring gene-coding mutations in Burkitt lymphoma and implicates ID3 as a new tumor suppressor gene.
2013-07-01 | GSE48435 | GEO