Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Hey3Met2 human ovarian cancer cells overexpressing wild type or catalytically-dead mutant RNASET2

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: marco fabbri 

PROVIDER: E-GEOD-28478 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Molecular signature induced by RNASET2, a tumor antagonizing gene, in ovarian cancer cells.

Acquati Francesco F   Monti Laura L   Lualdi Marta M   Fabbri Marco M   Sacco Maria Grazia MG   Gribaldo Laura L   Taramelli Roberto R  

Oncotarget 20110601 6

Using the Hey3Met2 human ovarian cancer cell line, we previously found the RNASET2 gene to possess a remarkable in vivo tumor suppressor activity, although no in vitro features such as inhibition of cell proliferation, clonogenic potential, impaired growth in soft agar and increase in apoptotic rate could be detected. This is reminiscent of the behavior of genes belonging to the class of tumor antagonizing genes (TAG) which act mainly within the context of the microenvironment. Here we present t  ...[more]

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