RNASET2-silenced and control OVCAR3 cell clones injected into nude mice.
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ABSTRACT:
PROVIDER: PRJNA184132 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the molecular pathways underlying RNASET2-mediated tumor suppression in vivo, we investigated the gene expression profile of tumor samples obtained from control and RNASET2-silenced OVCAR3 xenografts, respectively. In order to evaluate the contribution of human cancer cells and the murine host stroma to RNASET2-mediated tumorigenesis responses, total RNA extracted from tumor xenografts derived from six independent OVCAR3 cell clones (three parental and three RNASET2-silenced clones) was fluorescently labeled and hybridized to human Agilent whole-genome microarrays. Control and RNASET2-silenced OVCAR3 were injected subcutaneously into nude mice. After 39 days mice were sacrified, tumors were extracted and total RNA purified.
2013-05-01 | E-GEOD-43029 | biostudies-arrayexpress
Project description:To investigate the molecular pathways underlying RNASET2-mediated tumor suppression in vivo, we investigated the gene expression profile of tumor samples obtained from control and RNASET2-silenced OVCAR3 xenografts, respectively. In order to evaluate the contribution of human cancer cells and the murine host stroma to RNASET2-mediated tumorigenesis responses, total RNA extracted from tumor xenografts derived from six independent OVCAR3 cell clones (three parental and three RNASET2-silenced clones) was fluorescently labeled and hybridized to human Agilent whole-genome microarrays.
2013-05-01 | GSE43029 | GEO
Project description:Abstract/objective: RNASET2 is a lysosomal RNase whose enzymatic function is required for early events in lipotoxicity. However, the endogenous RNA substrates of RNASET2 that modulate lipid-induced cell death are not known. The purpose of this study was to identify RNASET2 substrates that impact lipotoxic stress. Methods: RNA sequencing was used to identify RNAs that increase in abundance in human cells upon RNASET2 knockdown, and actinomycin D assays were used to show that RNASET2 impacted decay rates of these RNAs. We tested for the presence of these RNAs in immunoisolated lysosomes and determined the contribution of the lysosomal membrane transporter SIDT2 in delivery of these RNAs to the lysosome. A role for these RNAs in lipotoxic cell death was directly tested in loss- and gain of function analysis. Results: RNASET2 knockdown increased steady-state abundance of UCHL3, PFN2 and PRDX3 mRNAs and prolonged their decay rate, leading to increased protein expression. These mRNAs were delivered to the lysosomal lumen by the lysosomal membrane transporter SIDT2 that mediates RNautophagy. While UCHL3 and PFN2 have not previously been implicated in lipotoxic responses, expression of these proteins protected against lipid-induced cell death. Conclusions: Our study identified specific mRNA substrates of RNASET2 and uncovered a previously unexplored function for lysosomes and RNautophagy in regulation of the response to metabolic stress. Moreover, we demonstrate that RNautophagy selectively regulates turnover of specific endogenous RNAs and thereby impacts regulation of gene expression.
2026-07-09 | GSE337307 | GEO
Project description:Abstract/objective: RNASET2 is a lysosomal RNase whose enzymatic function is required for early events in lipotoxicity. However, the endogenous RNA substrates of RNASET2 that modulate lipid-induced cell death are not known. The purpose of this study was to identify RNASET2 substrates that impact lipotoxic stress. Methods: RNA sequencing was used to identify RNAs that increase in abundance in human cells upon RNASET2 knockdown, and actinomycin D assays were used to show that RNASET2 impacted decay rates of these RNAs. We tested for the presence of these RNAs in immunoisolated lysosomes and determined the contribution of the lysosomal membrane transporter SIDT2 in delivery of these RNAs to the lysosome. A role for these RNAs in lipotoxic cell death was directly tested in loss- and gain of function analysis. Results: RNASET2 knockdown increased steady-state abundance of UCHL3, PFN2 and PRDX3 mRNAs and prolonged their decay rate, leading to increased protein expression. These mRNAs were delivered to the lysosomal lumen by the lysosomal membrane transporter SIDT2 that mediates RNautophagy. While UCHL3 and PFN2 have not previously been implicated in lipotoxic responses, expression of these proteins protected against lipid-induced cell death. Conclusions: Our study identified specific mRNA substrates of RNASET2 and uncovered a previously unexplored function for lysosomes and RNautophagy in regulation of the response to metabolic stress. Moreover, we demonstrate that RNautophagy selectively regulates turnover of specific endogenous RNAs and thereby impacts regulation of gene expression.
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Project description:RNASET2-deficient leukoencephalophathy is a severe leukodystrophy affecting children with psychomotor impairements in their forst year of life. We generated the first zebrafish model for a human leukodystrophy by targetting the ortholog rnaset2 gene using mutagenesis. This zebrafish mutant recapitulated the human clinical manisfestations and developed white matter defects detectable by MRI. Additionally, this zebrafish mutant identified this disease as a lysosomal storage disorders, with RNA accumulating in neurons. To understand how accumulation of RNA in neurons trigger white matter lesions, we undertook an unbiased approach and perfored microarray analysis. We identified differentially expressed genes in mutants and the immune system as a key pathway disregulated in the zebrafish rnaset2 mutant.
2019-10-08 | GSE138493 | GEO
Project description:Hey3Met2 cells were stably transfected with plasmids encoding either wild-type RNASET2 or a catalytically dead form (whose cDNA has been previously mutagenized in the two CAS catalytic sites) or with the empty vector as a control. The control of ovarian tumorigenesis by RNASET2 occurs through modification of the cellular microenvironment and involvement of immunocompetent cells, thus providing evidence for specific modulations of cellular responses induced by RNASET2 that might underlay ovarian tumorigenesis. In order to get more inside on the effect of RNASET2 on the modulation of other genes, a whole genome expression has been run on Hey3Met2 cell transfected with wildtype or mutated RNASET2.
2011-06-01 | GSE28478 | GEO
Project description:In order to illustrate the change of SW620 xenografts in nude mice, we collected SW620 xenografts at Week5 after the tumor cells were injected subcutaneously in nude mouse. Tumor tissues were collected and disocciated to single cells and subjected to scRNA-SEQ.
2026-02-11 | GSE269621 | GEO
Project description:Hey3Met2 cells were stably transfected with plasmids encoding either wild-type RNASET2 or a catalytically dead form (whose cDNA has been previously mutagenized in the two CAS catalytic sites) or with the empty vector as a control. The control of ovarian tumorigenesis by RNASET2 occurs through modification of the cellular microenvironment and involvement of immunocompetent cells, thus providing evidence for specific modulations of cellular responses induced by RNASET2 that might underlay ovarian tumorigenesis. In order to get more inside on the effect of RNASET2 on the modulation of other genes, a whole genome expression has been run on Hey3Met2 cell transfected with wildtype or mutated RNASET2. Hey3Met2 human ovarian cancer cells were transfected with espression vectors encoding either wild type or catalitycally dead mutant RNASET2. Clones transfected with the empty vectors were used as negative controls. Three independent clones were used for the each type of transfected plasmid.
2011-06-01 | E-GEOD-28478 | biostudies-arrayexpress
Project description:Ovarian cancer is the fifth most lethal malignancy in women, and epithelial ovarian cancer (EOC) is the most common histological type. Due to the absence of specific symptoms and diagnostic biomarkers, greater than 70% of EOC patients are diagnosed with clinical stage Federation International of Gynecology and Obstetrics (FIGO) III or IV, which has a five-year survival rate of only 20% to 30%. Thus, it is crucial to identify novel molecular biomarkers and therapeutic targets for EOC. NDC80 kinetochore complex component (NUF2) is upregulated and plays an important role in various human cancers. Our results showed that NUF2 was significantly upregulated in EOC tissues. Downregulation of NUF2 decreased cell proliferation, migration, invasion and tumor growth in nude mice. However, the mechanism of NUF2 in EOC remains unclear. The mechanisms by which NUF2 regulates EOC progression were detected by RNA sequencing. Thus, OVCAR3 cells after transfection with shNC (control) and shNUF2 (NUF2i) were added puromycin for establishing stable cell lines. RNA-seq was performed to analyze the differentially expressed genes in OVCAR3 cells after NUF2 knockdown.
2023-01-11 | GSE213611 | GEO
Project description:Muscle stem cells (MuSCs) fuse to form multinucleated cells to repair skeletal muscle after injury. While adult MuSCs express a cell autonomous myogenesis program, in vivo investigations demonstrated that the MuSC environment is required for efficient adult myogenesis and muscle regeneration. Particularly, anti-inflammatory/restorative macrophages stimulate MuSC differentiation and fusion, although the molecular mechanisms involved are still largely unknown. Here, we show that restorative macrophages secrete ribonuclease T2 (RNAseT2) which specifically stimulates MuSC fusion. Co-immuprecipitation coupled to mass spectrometry-based proteomics identified Ste20-like kinase (SLK) as binding partner of RNAseT2. SLK triggered the phosphorylation-mediated activation of N-WASP, allowing actin remodeling at the time of MuSC fusion.
2026-06-15 | PXD045581 | Pride