Ontology highlight
ABSTRACT:
PROVIDER: PRJNA986221 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25003548_1.fastq.gz | Fastqsanger.gz | |||
| SRR25003548_2.fastq.gz | Fastqsanger.gz | |||
| SRR25003549_1.fastq.gz | Fastqsanger.gz | |||
| SRR25003549_2.fastq.gz | Fastqsanger.gz | |||
| SRR25003550_1.fastq.gz | Fastqsanger.gz |
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Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks.
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Project description:Circular RNAs (circRNAs), a diverse class of ncRNAs highly enriched in developing neurons, play roles in local protein synthesis and synaptic plasticity. However, distinguishing functional from non-functional circRNAs is challenged by their abundance, tissue specificity and splicing variability. To address this, we conducted a RNAi knockdown screen targeting 32 highly expressed, conserved circRNAs enriched in dendritic processes. circRERE isoforms emerged as regulators of dendritic synapse density and electrophysiological characteristics. mRNA-seq supports the dysregulation of synaptic genes, particularly miR-128-3p-sensitive transcripts. MiR-128-3p activity and expression are reduced, with circRERE possessing multiple miR-128-3p binding sites, suggesting a protective interaction supported by a rescue of the synaptic phenotype upon miR-128-3p overexpression. Conversely, circRERE overexpression with intact miR-128-3p sites rescued the synaptic phenotype and independently increased miR-128-3p levels. These findings demonstrate the necessity for the broad characterization of circRNAs in the nervous system to comprehensively understand their influence on essential non-coding RNA regulatory networks.
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Project description:Circular RNAs (circRNAs), a diverse class of ncRNAs highly enriched in developing neurons, play roles in local protein synthesis and synaptic plasticity. However, distinguishing functional from non-functional circRNAs is challenged by their abundance, tissue specificity and splicing variability. To address this, we conducted a RNAi knockdown screen targeting 32 highly expressed, conserved circRNAs enriched in dendritic processes. circRERE isoforms emerged as regulators of dendritic synapse density and electrophysiological characteristics. mRNA-seq supports the dysregulation of synaptic genes, particularly miR-128-3p-sensitive transcripts. MiR-128-3p activity and expression are reduced, with circRERE possessing multiple miR-128-3p binding sites, suggesting a protective interaction supported by a rescue of the synaptic phenotype upon miR-128-3p overexpression. Conversely, circRERE overexpression with intact miR-128-3p sites rescued the synaptic phenotype and independently increased miR-128-3p levels. These findings demonstrate the necessity for the broad characterization of circRNAs in the nervous system to comprehensively understand their influence on essential non-coding RNA regulatory networks.
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Project description:Microglia were derived from iPSCs and treated with mimics and inhibitors of the miRNAs hsa-miR-150-5p, hsa-miR-193a-3p and hsa-miR-19b-3p. RNA-sequencing was then performed to examine the effects of up- and down-regulation of the respective miRNAs.
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Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks. Experimental design for mass spectrometry SILAC experiments can be found at https://figshare.com/s/8e79f008e0e58ec6efc2 or https://doi.org/10.6084/m9.figshare.4888139
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Project description:The loss of fragile X mental retardation protein (FMRP) causes fragile X syndrome (FXS), the most common inherited intellectual disability. How the loss of FMRP alters protein expression and astroglial functions remains essentially unknown. Here we showed that selective loss of astroglial FMRP in vivo up-regulates a brain-enriched miRNA, miR-128-3p, in mouse and human FMRP-deficient astroglia, which suppresses developmental expression of astroglial metabotropic glutamate receptor 5 (mGluR5), a major receptor in mediating developmental astroglia to neuron communication. Selective in vivo inhibition of miR-128-3p in FMRP-deficient astroglia sufficiently rescues decreased mGluR5 function, while astroglial overexpression of miR-128-3p strongly and selectively diminishes developmental astroglial mGluR5 signaling. Subsequent transcriptome and proteome profiling further suggests that FMRP commonly and preferentially regulates protein expression through posttranscriptional, but not transcriptional, mechanisms in astroglia. Overall, our study defines an FMRP-dependent cell-autonomous miR pathway that selectively alters developmental astroglial mGluR5 signaling, unveiling astroglial molecular mechanisms involved in FXS pathogenesis.
2020-09-10 | GSE157724 | GEO
Project description:The loss of fragile X mental retardation protein (FMRP) causes fragile X syndrome (FXS), the most common inherited intellectual disability. How the loss of FMRP alters protein expression and astroglial functions remains essentially unknown. Here we showed that selective loss of astroglial FMRP in vivo up-regulates a brain-enriched miRNA, miR-128-3p, in mouse and human FMRP-deficient astroglia, which suppresses developmental expression of astroglial metabotropic glutamate receptor 5 (mGluR5), a major receptor in mediating developmental astroglia to neuron communication. Selective in vivo inhibition of miR-128-3p in FMRP-deficient astroglia sufficiently rescues decreased mGluR5 function, while astroglial overexpression of miR-128-3p strongly and selectively diminishes developmental astroglial mGluR5 signaling. Subsequent transcriptome and proteome profiling further suggests that FMRP commonly and preferentially regulates protein expression through posttranscriptional, but not transcriptional, mechanisms in astroglia. Overall, our study defines an FMRP-dependent cell-autonomous miR pathway that selectively alters developmental astroglial mGluR5 signaling, unveiling astroglial molecular mechanisms involved in FXS pathogenesis.
2020-09-10 | GSE157723 | GEO
Project description:Friedreich’s ataxia (FRDA; OMIM 229300), an autosomal recessive neurodegenerative mitochondrial disease, is the most prevalent hereditary ataxia. In addition, FRDA patients showed additional non-neurological features such as scoliosis, diabetes and cardiac complications. Hypertrophic cardiomyopathy, which is found in two thirds of patients at the time of diagnosis, is the primary cause of death in these patients. In this data set, using small RNA-sequencing of small RNA purified from plasma samples of FRDA patients and controls we identified differential expression of miRNAs (hsa-miR-128-3p, hsa-miR-625-3p, hsa-miR-130b-5p, hsa-miR-151a-5p, hsa-miR-330-3p, hsa-miR-323a-3p, and hsa-miR-142-3p) between both groups. In addition, we found that miR-323a-3p can be used as a biomarker for differentiation of FRDA patients with cardiac problems. Identification of miRNA signatures could therefore provide new molecular explanation for pathological mechanisms occurring during the natural history of the FRDA. Since miRNA levels change with disease progression and pharmacological interventions, miRNAs will contribute to design new therapeutic strategies and improve clinical decisions.
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