Differential gene expression analysis between miR-17 overexpressing and control human chondrocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE279568 | GEO | 2025/10/16
REPOSITORIES: GEO
Similar Datasets
Project description:Differential gene expression analysis between miR-17 overexpressing and control human chondrocytes
| PRJNA1173523 | ENA
Project description:The synergism between c-MYC and miR-17-19b, a truncated version of the miR-17-92 cluster, is well documented during tumor initiation. However, little is known about miR-17-19b function in established cancers. Here we investigate the role of miR-17-19b in c-MYC-driven lymphomas by integrating SILAC-based quantitative proteomics, transcriptomics and 3’ UTR analysis upon miR-17-19b overexpression. We identify over one hundred novel miR-17-19b targets, of which 40% are co-regulated by c-MYC. Down-regulation of a new miR-17/20 target Chek2 increases the recruitment of HuR to c-MYC transcripts, resulting in the inhibition of c-MYC translation and thus interfering with in vivo tumor growth. Hence, in established lymphomas, miR-17-19b fine-tunes c-MYC activity through a tight control of its function and expression, ultimately ensuring cancer cell homeostasis. Our data highlight the plasticity of miRNA function, reflecting changes in the mRNA landscape and 3’ UTR shortening at different stages of tumorigenesis.
2015-11-06 | PXD002810 | Pride
Project description:To unravel the molecular mechanism underlying miR-17∼92 costimulatory function, we performed RNA-seq on CD4+ T cells from mice lacking miR-17∼92 in T cell, wildtype mice and mice overexpressing miR-17∼92 in T cells, in naïve state or activated vitro for 24h and 48h.
2022-09-08 | GSE140525 | GEO
Project description:Adult beta cells in the pancreas are the sole source of insulin in our body. Beta cell loss or increased demand for insulin, impose metabolic challenges because adult beta cells are generally quiescent and infrequently re-enter the cell division cycle. miR-17-92/106b is a family of proto-oncogene microRNAs, that regulate proliferation in normal tissues and in cancer. Here, we employ mouse genetics to demonstrate a critical role for miR-17-92/106b in glucose homeostasis and in controlling insulin secretion. Mass spectrometry analysis was performed on miR-17-92LoxP/LoxP;106-25-/- MEF lysate, without or with CRE-Adenovirus. miR-17-92LoxP/LoxP;106-25+/+ MEFs with GFP-Adenovirus served as controls. We demonstrate that miR-17-92/106b regulate the adult beta cell mitotic checkpoint and that miR-17-92/106b deficiency results in reduction in beta cell mass in-vivo. Furthermore, protein kinase A (PKA) is a new relevant molecular pathway downstream of miR-17-92/106b in control of adult beta cell division and glucose homeostasis. Therefore, contributes to the understanding of proto-oncogene miRNAs in the normal, untransformed endocrine pancreas, and illustrates new genetic means for regulation of beta cell mitosis and function by non-coding RNAs.
2019-06-17 | PXD012610 | Pride
Project description:Analysis of mouse chondrocytes lacking the microRNA-140. MicroRNAs are genomically encoded small RNAs to regulate the gene expression. miR-140 shows high expression in cartilage. Results provide insight into the molecular mechanisms underlying miR-140 function in chondrocytes. Keywords: Expression profiling by array
2010-01-01 | GSE16007 | GEO
Project description:To unravel the molecular mechanism underlying miR-17∼92 costimulatory function, we performed RNA-seq on CD4+ T cells from mice lacking miR-17∼92 in T cell, wildtype mice, mice overexpressing miR-17∼92 in T cells , mice with a constitutive knockout of CD28, and rescue mice, in naïve state or activated vitro for 24h.
2022-09-08 | GSE140564 | GEO
Project description:A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain the gene expression pattern during hematopoiesis. In this network transcription factors regulate each other and are involved in regulatory loops with microRNAs.The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes for six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.
2021-09-09 | PXD018052 | Pride
Project description:Emerging evidence has shown that noncoding RNAs, particularly microRNAs (miRNAs), contribute to the pathogenesis of mood and anxiety disorders, although the molecular mechanisms are poorly understood. Here we show altered levels of miR-17-92 in adult hippocampal neural progenitors have a significant impact in neurogenesis and anxiety- and depression-related behaviors in mice. miR-17-92 deletion in adult neural progenitors causes a decrease, while its overexpression an increase of neurogenesis in the dentate gyrus, through regulating genes in the glucocorticoid pathway, especially serum- and glucocorticoid-inducible protein kinase-1 (Sgk1). miR-17-92 knockout mice show anxiety- and depression-like behaviors, whereas miR-17-92 overexpressing mice exhibit anxiolytic and antidepression-like behaviors. Furthermore, we show that miR-17-92 expression in the adult mouse hippocampus responds to chronic stress, and miR-17-92 rescues proliferation defects, induced by corticosterone, in hippocampal neural progenitors. Our study uncovers a crucial role for miR-17-92 in adult neural progenitors to regulate neurogenesis and anxiety- and depression-like behaviors.
2016-12-09 | GSE83636 | GEO
Project description:Analysis of mouse chondrocytes lacking the microRNA-140. MicroRNAs are genomically encoded small RNAs to regulate the gene expression. miR-140 shows high expression in cartilage. Results provide insight into the molecular mechanisms underlying miR-140 function in chondrocytes. Keywords: Expression profiling by array DNA microarray analysis was performed using Affymetrix mouse genome 430 2.0 array. RNA samples collected from cultured rib chondrocytes of wild-type and miR-140-/- to identify potential mRNA targets of miR-140. 2 M-BM-5g of total RNA was reverse transcribed with SuperScript II and second strand cDNA was synthesized. Biotinylated antisense cRNAs was amplified and transcribed using the GeneChip expression 3M-bM-^@M-^Y-Amplification reagent (Affymetrix). Finally, 10 M-BM-5g of cRNAs were fragmented and hybridized to GeneChip (R) Mouse Genome 430 2.0 array (Affymetrix). Microarray data were summarized by Robust Multichip Average (RMA) method and statistical analysis was performed using NIA Array Analysis (http://Igusun.grc.nia.nih.gov/ANOVA/).
2010-01-01 | E-GEOD-16007 | biostudies-arrayexpress
Project description:mRNA profiles of primary mouse chondrocytes transfected with miR-Ctrl or miR-204 mimics were generated by mRNA sequencing. This study provides insights into the role of miR-204 in chondrocytes.
2019-02-22 | GSE126846 | GEO