MCF-7 serum withdrawal (Agilent mouse 60K microarray)
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ABSTRACT:
PROVIDER: PRJNA1163901 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MCF-7 cordycepin treatment (Agilent mouse 60K microarray)
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Project description:NIH3T3 serum stimulation and cordycepin treatment (Agilent mouse 60K microarray)
| PRJNA1162803 | ENA
Project description:3’deoxyadenosine, also known as cordycepin, has been widely researched as a potential treatment for cancer, yielding promising results in tissue culture as well as in pre-clinical models. A wide variety of mechanisms of action have been proposed, with little agreement between different studies. Here, we confirm that cordycepin triphosphate is likely to be the active metabolite of cordycepin. Data from single and high throughput experiments showed that cordycepin represses growth factor induced gene expression. Bioinformatic analysis, quantitative PCR and western blotting confirmed that cordycepin blocks the PI3K/AKT/mTOR and/or MEK/ERK pathways in 6 cell lines. Effects of cordycepin on translation through mTOR pathway repression were detectable within 30 minutes, indicating a rapid process. Our data show that cordycepin has a broadly similar mechanism of action in all cell lines studied and indicate that its therapeutic target is a cordycepin triphosphate sensitive molecule that is required for growth factor signal transduction.
2025-02-19 | GSE277763 | GEO
Project description:Agilent SurePrint G3 Mouse GE V2.0 Microarray(8*60K,Design ID:074809)
| PRJNA699158 | ENA
Project description:Fulvestrant withdrawal from fulvestrant-resistant MCF-7/FR cells
| PRJNA497213 | ENA
Project description:To understand the regulatory relationships among EC transcripts during apoptosis using serum withdrawal time series microarray data and use this to identify master regulators of endothelial cell apoptosis.
2012-07-20 | GSE23067 | GEO
Project description:To understand the regulatory relationships among EC transcripts during apoptosis using serum withdrawal time series microarray data and use this to identify master regulators of endothelial cell apoptosis. In the study presenty here, HUVEC isolates from 10 different individuals were pooled. The extracted RNA was hybridised onto the microarray at different timepoints following treatment with serum withdrawal. The time course was replicated 3 times using three different pools of 10 HUVEC isolates.
2012-07-19 | E-GEOD-23067 | biostudies-arrayexpress
Project description:Estrogens have been shown to elicit anti-cancer effects against estrogen receptor alpha (ER)-positive breast cancer. We sought to determine the underlying mechanism of therapeutic response. Response to 17b-estradiol was assessed in ER+ breast cancer models with resistance to estrogen deprivation: WHIM16 patient-derived xenografts, C7-2-HI and C4-HI murine mammary adenocarcinomas, and long-term estrogen-deprived MCF-7 cells. As another means to reactivate ER, the anti-estrogen fulvestrant was withdrawn from fulvestrant-resistant MCF-7 cells. Transcriptional, growth, apoptosis, and molecular alterations in response to ER reactivation were measured. 17b-estradiol treatment and fulvestrant withdrawal induced transcriptional activation of ER, and cells adapted to estrogen deprivation or fulvestrant were hypersensitive to 17b-estradiol. ER transcriptional response was followed by an unfolded protein response and apoptosis. Such apoptosis was dependent upon the unfolded protein response, p53, and JNK signaling. Anti-cancer effects were most evident in models exhibiting genomic amplification of the gene encoding ER (ESR1), suggesting that engagement of ER at high levels is cytotoxic. These data indicate that long-term adaptation to estrogen deprivation or ER inhibition alters sensitivity to ER reactivation. In such adapted cells, 17b-estradiol treatment and anti-estrogen withdrawal hyperactivate ER, which drives an unfolded protein response activation and subsequent growth inhibition and apoptosis. 17b-estradiol treatment should be considered as an alternative therapy for anti-estrogen-resistant disease, particularly in patients with tumors harboring ESR1 amplification or overexpression. Furthermore, therapeutic strategies that enhance an unfolded protein response may enhance the therapeutic effects of ER reactivation.
2019-08-19 | GSE121379 | GEO
Project description:3’deoxyadenosine, also known as cordycepin, has been widely researched as a potential treatment for cancer, yielding promising results in tissue culture as well as in pre-clinical models. A wide variety of mechanisms of action have been proposed, with little agreement between different studies. Here, we confirm that cordycepin triphosphate is likely to be the active metabolite of cordycepin. Data from single and high throughput experiments showed that cordycepin represses growth factor induced gene expression. Bioinformatic analysis, quantitative PCR and western blotting confirmed that cordycepin blocks the PI3K/AKT/mTOR and/or MEK/ERK pathways in 6 cell lines. Effects of cordycepin on translation through mTOR pathway repression were detectable within 30 minutes, indicating a rapid process. Our data show that cordycepin has a broadly similar mechanism of action in all cell lines studied and indicate that its therapeutic target is a cordycepin triphosphate sensitive molecule that is required for growth factor signal transduction.
2025-02-19 | GSE277620 | GEO
Project description:Total RNA was quantified by the NanoDrop ND-2000 (Thermo Scientific)and the RNA integrity was assessed using Agilent Bioanalyzer 2100 (Agilent Technologies). The sample labeling, microarray hybridization and washing were performed based on the manufacturer's standard protocols. Briefly, total RNA were transcribed to double strand cDNA, then synthesized into cRNA and labeled with Cyanine-3-CTP. The labeled cRNAs were hybridized onto the microarray. After washing, the arrays were scanned by the Agilent Scanner G2505C (Agilent Technologies).
2021-02-04 | GSE166057 | GEO