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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Colon cancer shperes are sensitive to Fenretinide

ABSTRACT: Fenretinide has shown its antitumor activity in many tumor types with low cytotoxicity to normal cells. Recently, we have shown that fenretinide could eradicate chronic myeloid leukemia stem/progenitor cells and spheres from ovarian cancer. In this study, we investigate whether fenretinide could selectively target sphere cells of colon cancer. Using high-throughtput microarray system, we identified GO terms and pathway signatures enriched in fenretinide treated HT29 cells and HT29 derived sphere cells. Colon cancer cells HT29 were cultured in sphere formation conditions, HT29 cells and HT29 derived sphere cells were treated with fenretinide, and total RNA from those spheres and corresponding adhered cell was hybridized on Affymetrix U133 plus 2.0 genechip.

ORGANISM(S): Homo sapiens

SUBMITTER: Jiansheng Liu

PROVIDER: E-GEOD-66983 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Colon cancer shperes are sensitive to Fenretinide

Project description:Fenretinide has shown its antitumor activity in many tumor types with low cytotoxicity to normal cells. Recently, we have shown that fenretinide could eradicate chronic myeloid leukemia stem/progenitor cells and spheres from ovarian cancer. In this study, we investigate whether fenretinide could selectively target sphere cells of colon cancer. Using high-throughtput microarray system, we identified GO terms and pathway signatures enriched in fenretinide treated HT29 cells and HT29 derived sphere cells.

2016-04-03 | GSE66983 | GEO

Identify the cancer stem cells expression characteristics in ovarian and breast cancer

Project description:The identification and characterization of subpopulations of cancer stem cells (CSCs) provide new understandings and possible therapeutic implications in cancer biology. We found the ovarian cancer sphere cells possessed CSCs properties maintained self renewal, drug resistance, and tumorigenesis. Using high-throughput microarray system, we identified common GO terms and pathway signatures significantly enriched in ovarian and breast cancer stem cells. Ovarian and breast cancer cells were cultured in sphere formation conditions, and total RNA from those spheres and conresponding adhered cell was hybridized on Affymetrix microarrays.

2013-11-25 | E-GEOD-43657 | biostudies-arrayexpress

Comparison of gene expression levels in parental U87 cells and U87 tumor spheres treated with or without ITE

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2015-04-18 | E-GEOD-67986 | biostudies-arrayexpress

Expression data of rhabdomyosarcoma cells and spheres

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2011-04-30 | E-GEOD-26635 | biostudies-arrayexpress

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2015-03-04 | E-GEOD-65499 | biostudies-arrayexpress

Human acute myelogenous leukemia-initiating cells treated with fenretinide

Project description:Transcriptional profiling of human acute myelogenous leukemia (AML) CD34+ cells treated with 5 μM fenretinide. Two timepoints included are 6h, 12h, covering the apoptosis-induction time window of AML CD34+ cells responsing to the fenretinide treatment. We studied gene expression series in human AML CD34+ cells with or without 5 μM fenretinide treatment by cDNA microarray analysis. Several signal transduction pathways are involve, including stress response, NF-kappaB inhibition and p53 inhibition (p<0.05). These findings indicate fenretinide may represent a promising candidate for targeting AML-initiating cells. 6-condition experiment, untreated AML CD34+ cells vs. fenretinide-treated AML CD34+ cells,including 2 time points, for each point the untreated and 5 μM fenretinide treated, independently grown and harvested. Untreated was used to counteracting the background.

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Time-series transcriptome profilings of control and Fenretinide-treated human NB4 cells

Project description:Pharmacological intervention of redox balance in cancer cells often results in oxidative stress-mediated apoptosis, attracting much attention for the development of a new generation of targeted therapy in cancer. However, little is known about mechanisms underlying the conversion from oxidative signaling to downstream activities leading cells to death. We here report a systematic detection of transcriptome changes in response to oxidative signals generated in leukemia cells upon fenretinide treatment, implicating the occurrence of numerous stress-responsive events during the fenretinide induced apoptosis, such as redox response, endoplasmic reticulum stress/unfolded protein response, translational repression and proteasome activation. Moreover, the configuration of these relevant events is primarily orchestrated by stress responsive transcription factors, as typically highlighted by NF-E2-related factor-2 (NRF2) and heat shock factor 1 (HSF1). Several lines of evidence suggest that the coordinated regulation of these transcription factors and thus their downstream genes are involved in converting oxidative signaling into downstream stress-responsive events regulating pro-apoptotic and apoptotic activities at the temporal and spatial levels, typifying oxidative stress-mediated programmed death rather than survival in cancer cells. This study provides a roadmap for understanding oxidative stress-mediated apoptosis in cancer cells, which may be further developed into more sophisticated therapeutic protocols, as implicated by synergistic induction of cell apoptosis using proteasome inhibitors with fenretinide. Time-series experiment, fenretinide treated NB4 cells at 19 time points (i.e., 0.25, 0.5, 1, 2, 4, 6, 8, 10, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54 and 60 hours) and untreated NB4 cells at 4 time points (i.e., 0, 8, 12 and 15 hours).

2010-05-05 | E-GEOD-16578 | biostudies-arrayexpress

Transcription profiling of human untreated and fenretinide-treated CD34+ cells from 4 CML patients

Project description:Imatinib therapy is first-line treatment for chronic myeloid leukemia (CML), and its failure to target CML progenitor/stem cells may lead to an increased risk of relapse. We report here that fenretinide, a well-tolerated vitamin A derivative, is capable of eradicating primitive CML progenitor/stem cells and significantly enhances the efficacy of imatinib at physiologically achievable concentrations. As tested by colony forming cell assays, formation of various colonies derived primitive CML CD34+ cells was significantly suppressed by fenretinide, particularly with respect to the formation of colonies derived from erythroid progenitors and more primitive CML progenitor/stem cells. Also, fenretinide significantly enhanced the ability of imatinib to suppress the formation of the colonies. Moreover, fenretinide was able to induce apoptosis in primitive CML CD34+ cells while sparing the normal counterparts. In particular, primitive CML CD34+CD38- cells appeared to be most sensitive to fenretinide induced apoptosis. Through transcriptome analysis and molecular validation, we further showed that fenretinide induced apoptosis in CML CD34+ cells was probably mediated by a series of stress responsive events which were likely triggered by elevated levels of intracellular reactive oxygen species. Accordingly, the combination of fenretinide and imatinib may provide a potential solution for overcoming relapse and resistance in CML. Experiment Overall Design: Transcriptome profiles of CML CD34+ cells with and without fenretinide treatment were analyzed using whole genome expression arrays (Affymetrix HG-U133 Plus 2.0) in four CML patients (CML32, CML33, CML34 and CML35, see Table 1). To minimize potential data biases, both treated and untreated cell samples were maintained in culture for 48 hours before hybridization.

2009-12-05 | E-GEOD-17480 | biostudies-arrayexpress

Expression data from breast cancer tumor-initiating cells

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2012-12-21 | E-GEOD-32526 | biostudies-arrayexpress

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2012-12-15 | E-GEOD-42066 | biostudies-arrayexpress

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