ASNase treatment in PC3 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE74510 | GEO | 2016/02/17
SECONDARY ACCESSION(S): PRJNA300627
REPOSITORIES: GEO
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Project description:Ribosome profiling performed on control and L-Asparaginase treated PC3 cells 2 individual batches: (i) 1 control and 1 treated sample, (ii) 1 control and 2 treated samples
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2017-01-31 | GSE94289 | GEO
Project description:To integrate genome-wide occupancy of canonical and ncPRC1 with control of gene expression, we performed ChIPseq analysis for RNF2 (cPRC1 and ncPRC1), BMI1 and PHC2 (cPRC1), and KDM2B (ncPRC1.1) and integrated the results with the known occupancy data for the transcriptional repression mark H3K27me3 and the activation mark H3K4me3 in PC3 cells. Finally, we show that the capacity of PRC1 is to positively control the gene expression associated with the acquisition of mesenchymal and stem-like traits and progression to metastasis in PC3.
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Project description:Resistance to asparaginase, an antileukemic enzyme that depletes asparagine, is a common clinical problem. Using a genome-wide CRISPR/Cas9 screen, we found a synthetic lethal interaction between Wnt pathway activation and asparaginase in acute leukemias resistant to this enzyme. Wnt pathway activation induced asparaginase sensitivity in distinct treatment-resistant subtypes of acute leukemia, but not in normal hematopoietic progenitors. Sensitization to asparaginase was mediated by Wnt-dependent stabilization of proteins (Wnt/STOP), which inhibits GSK3-dependent protein ubiquitination and proteasomal degradation, a catabolic source of asparagine. Inhibiting the alpha isoform of GSK3 phenocopied this effect, and pharmacologic GSK3 inhibition profoundly sensitized drug-resistant leukemias to asparaginase. Our findings provide a molecular rationale for activation of Wnt/STOP signaling to improve the therapeutic index of asparaginase. To gain further insights into mechanisms of cytotoxicity of this combination, we applied unbiased mass spectrometry proteomics to CCRF-CEM cells, a human T-cell acute lymphoblastic leukemia cell line, treated with vehicle, asparaginase alone, the GSK3 inhibitor BRD0705 (which phenocopies Wnt/STOP pathway activation), or the combination of asparaginase and BRD0705.
2019-03-29 | PXD013061 | Pride
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Project description:We compared PC3 cells with or without harboring the wild-AR construct in the growth conditions of 1nM R1881, 10nM R1881 and ethanol (the solvent for R1881). The MOCK control is PC3 cells transfected with the empty vectors. Experiment Overall Design: 2 PC3 Samples transfected with empty vector, without R1881, 2 PC3 Samples transfected with AR, treated with Ethanol, 2 PC3 Samples transfected with AR, treated with 1nM R1881, 1 PC3 transfected with AR, treated with 10nM R1881.
2009-03-15 | E-GEOD-15091 | biostudies-arrayexpress
Project description:It is aimed to reveal overall trancriptional change in prostate cancer PC3 cells after ectopic expression of miR-145 Pre-mir-145 transfected PC3 cells were collected at 8, 16 and 24 hours after transfection and control untrasfected PC3 cells were used.
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Project description:Differential complementary positional prroteomics of human carboxypeptidase 4 treated PC3-lysates
2010-05-19 | PRD000228 | Pride
Project description:BACKGROUND: Cancer stem-like cells are proposed to sustain solid tumors by virtue of their capacity for self-renewal and differentiation to cells that comprise the bulk of the tumor, and have been identified for a variety of cancers based on characteristic clonal morphologies and patterns of marker gene expression. METHODS: Single cell cloning and spheroid culture studies were used to identify a population of cancer stem-like cells in the androgen-independent human prostate cancer cell line PC3. RESULTS: We demonstrate that, under standard culture conditions, ~10% of PC3 cells form holoclones with cancer stem cell characteristics. These holoclones display high self-renewal capability in spheroid formation assays under low attachment and serum-free culture conditions, retain their holoclone morphology when passaged at high cell density, exhibit moderate drug resistance, and show high tumorigenicity in scid immunodeficient mice. PC3 holoclones readily form spheres, and PC3-derived spheres yield a high percentage of holoclones, further supporting their cancer stem cell-like nature. We identified one gene, FAM65B, whose expression is consistently up regulated in PC3 holoclones compared to paraclones, the major cell morphology in the parental PC3 cell population, and two genes, MFI2 and LEF1, that are consistently down regulated. This molecular profile, FAM65Bhigh/MFI2low/LEF1low, also characterizes spheres generated from parental PC3 cells. The PC3 holoclones did not show significant enriched expression of the putative prostate cancer stem cell markers CD44 and integrin α2β1. PC3 tumors seeded with holoclones showed dramatic down regulation of FAM65B and dramatic up regulation of MFI2 and LEF1, and unexpectedly, a marked increase in tumor vascularity compared to parental PC3 tumors, suggesting a role of cancer stem cells in tumor angiogenesis. CONCLUSIONS: These findings support the proposal that PC3 tumors are sustained by a small number of tumor-initiating cells with stem-like characteristics, including strong self-renewal and pro-angiogenic capability and marked by the expression pattern FAM65Bhigh/MFI2low/LEF1low. These markers may serve as targets for therapies designed to eliminate cancer stem cell populations associated with aggressive, androgen-independent prostate tumors such as PC3. (Mol Cancer. 2010 Dec 29;9:319. doi: 10.1186/1476-4598-9-319; PMID: 21190562; PMCID: PMC3024252).
2013-11-07 | GSE52161 | GEO