The Expression profile of splenic/hepatic macrophages in RNaseT2 deficient mice
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ABSTRACT:
PROVIDER: PRJNA1185141 | 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.
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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.
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