The Splicing Factor SF2 is Critical for Hyperproliferation and Survival in a TORC1-Dependent Model of Early Tumorigenesis in Drosophila
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PROVIDER: PRJEB39006 | ENA |
REPOSITORIES: ENA
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Project description: Not available
| S-EPMC7352841 | biostudies-literature
Project description:Mice developed ovarian tumors after Arid1a and Pten double knockout. Gene expression profiles of 5 such ovarian tumors were compared with those of 4 normal ovaries. The differentially expressed genes were then used to investigate the similarity between the mouse ovarian tumors and major subtypes of human ovarian cancers. Total RNA obtained from the mouse ovarian tumors developing after Arid1a and Pten knockout compared to normal mouse ovaries.
2014-04-05 | E-GEOD-56531 | biostudies-arrayexpress
Project description:Autophagy is a conserved process of cellular self-digestion that promotes survival during nutrient stress. In yeast, methionine starvation is sufficient to induce autophagy. One pathway of autophagy induction is governed by the SEACIT complex, which regulates TORC1 activity in response to amino acids through the Rag GTPases Gtr1 and Gtr2 This work identifies an unexpected yet critical role for Xrn1 in nutrient sensing and growth control that extends beyond its canonical housekeeping function in RNA degradation and indicates an avenue for RNA metabolism to function in amino acid signaling into TORC1.
2023-10-19 | GSE226779 | GEO
Project description:Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated expression of wild type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53-) mice. By comparing morphology and gene expression profiles in the Trp53+ and Trp53- OSE cells, we document that wild-type TRP53 acts as a major promoter of OSE cell survival and differentiation: cells lacking Trp53 are transformed yet are less adherent, migratory and invasive and exhibit a gene expression profile more like normal OSE cells. These results provide a new paradigm: wild type TRP53 does not preferentially induce apoptotic or senescent related genes in the Pten;Kras(Trp53+) cancer cells but rather increases genes regulating DNA repair, cell cycle progression and proliferation and decreases putative tumor suppressor genes. However, if TRP53 activity is forced higher by exposure to nutlin-3a (an MDM2 antagonist), TRP53 suppresses DNA repair genes and induces the expression of genes that control cell cycle arrest and apoptosis. Thus, in the Pten;Kras(Trp53+) mutant mouse OSE cells and likely in human TP53+ low grade ovarian cancer cells, wild type TRP53 controls global molecular changes that are dependent on its activation status. These results suggest that activation of TP53 may provide a promising new therapy for managing type I ovarian cancer and other cancers in humans where wild-type TP53 is expressed. A direct comparison of ovarian surface epithelia cells from three different genotype mice
2012-06-20 | E-GEOD-34882 | biostudies-arrayexpress
Project description:Snf1 and TORC1 are two global regulators that sense the nutrient availability and regulate the cell growth in yeast Saccharomyces cerevisiae. Here we undertook a systems biology approach to study the effect of deletion of these genes and investigate the interaction between Snf1 and TORC1 in regulation of gene expression and cell metabolism.
2011-10-20 | GSE24421 | GEO
Project description:Leishmania TORC1 links nutrient availability to differentiation into infective
2022-10-31 | MSV000090621 | MassIVE
Project description:Recent publications have described an important role for cross talk between PI-3 kinase and sonic hedgehog signaling pathways in the pathogenesis of medulloblastoma. Our primary objective was to determine if loss of Pten promotes medulloblastoma tumor formation. When mice expressing SmoA1 were crossed with mice heterozygous for Pten, SmoA1 +; Pten +/- mice exhibited decreased survival, an increased incidence, and a shorter time to onset of symptoms, compared to SmoA1 +; Pten +/+ mice. Tumors from SmoA1 +; Pten +/+ mice exhibited classic histology. In contrast, tumors from SmoA1 +; Pten +/- mice exhibited predominantly nodular/desmoplastic histology and evidence of neuronal differentiation. Analysis by gene expression microarray revealed a clear separation of gene signatures, with upregulation of genes such as Pik3cb, Mapk8, Frap1, and multiple genes involved in angiogenesis in SmoA1+; Pten +/- tumors. Downregulated genes included Pten, Trp53, and Rb1. Western blotting and immunohistochemical analysis revealed decreased expression of Pten and increased activation of Akt in the SmoA1+; Pten +/- tumors. Consistent with these findings, we detected strong expression of PCNA throughout the Pten +/+ tumors and focal areas of intense staining for PCNA in tumors from SmoA1 +/-; Pten +/- mice. Conversely, staining for Cleaved Caspase 3 revealed multiple punctuate foci in SmoA1 +; Pten +/+ tumors and almost no staining in SmoA1 +/-; Pten +/- tumors. These results suggest that increased signaling through PI-3 kinase pathways promotes MB tumorigenesis by driving proliferation and inhibiting apoptosis of granule neuron precursor cells in the developing cerebellum.
2009-11-21 | GSE19059 | GEO
Project description:Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated expression of wild type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53-) mice. By comparing morphology and gene expression profiles in the Trp53+ and Trp53- OSE cells, we document that wild-type TRP53 acts as a major promoter of OSE cell survival and differentiation: cells lacking Trp53 are transformed yet are less adherent, migratory and invasive and exhibit a gene expression profile more like normal OSE cells. These results provide a new paradigm: wild type TRP53 does not preferentially induce apoptotic or senescent related genes in the Pten;Kras(Trp53+) cancer cells but rather increases genes regulating DNA repair, cell cycle progression and proliferation and decreases putative tumor suppressor genes. However, if TRP53 activity is forced higher by exposure to nutlin-3a (an MDM2 antagonist), TRP53 suppresses DNA repair genes and induces the expression of genes that control cell cycle arrest and apoptosis. Thus, in the Pten;Kras(Trp53+) mutant mouse OSE cells and likely in human TP53+ low grade ovarian cancer cells, wild type TRP53 controls global molecular changes that are dependent on its activation status. These results suggest that activation of TP53 may provide a promising new therapy for managing type I ovarian cancer and other cancers in humans where wild-type TP53 is expressed.
2012-06-21 | GSE34882 | GEO
Project description:Mice developed ovarian tumors after Arid1a and Pten double knockout. Gene expression profiles of 5 such ovarian tumors were compared with those of 4 normal ovaries. The differentially expressed genes were then used to investigate the similarity between the mouse ovarian tumors and major subtypes of human ovarian cancers.
2014-04-05 | GSE56531 | GEO
Project description:Snf1 and TORC1 are two global regulators that sense the nutrient availability and regulate the cell growth in yeast Saccharomyces cerevisiae. Here we undertook a systems biology approach to study the effect of deletion of these genes and investigate the interaction between Snf1 and TORC1 in regulation of gene expression and cell metabolism. 3 mutant strains (snf1?, tor1?, snf1?tor1?) together with 1 reference strain grown under both glucose-limited or amonia-limited defined media with three biological replicates for each strain
2011-10-19 | E-GEOD-24421 | biostudies-arrayexpress