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Effect of glucose refeeding after short-term glucose withdrawal on gene expression of MCF7 cells

ABSTRACT: Effect of glucose refeeding after short-term glucose withdrawal on gene expression of MCF7 cells

PROVIDER: PRJNA850427 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19737219_1.fastq.gz	Fastqsanger.gz
	SRR19737219_2.fastq.gz	Fastqsanger.gz
	SRR19737220_1.fastq.gz	Fastqsanger.gz
	SRR19737220_2.fastq.gz	Fastqsanger.gz
	SRR19737221_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Effect of glucose refeeding after short-term glucose withdrawal on gene expression of MCF7 cells

Project description:MCF7 is an epithelial cell line isolated from the breast tissue of a patient with metastatic adenocarcinoma. Growth factors are well-known stimulators of glycometabolism. Whether glucose autoregulates its own metabolism remains poorly understood. To probe this, we designed the glucose-refeeding experiment in MCF7 for RNAseq analysis.

2023-06-29 | GSE206394 | GEO

Effect of short-term glucose withdrawal and glucose refeeding after short-term glucose withdrawal on gene expression of MCF7 cells

Project description:Effect of short-term glucose withdrawal and glucose refeeding after short-term glucose withdrawal on gene expression of MCF7 cells

| PRJNA850424 | ENA

Effect of short-term glucose withdrawal on gene expression of MCF7 cells

Project description:MCF7 is an epithelial cell line isolated from the breast tissue of a patient with metastatic adenocarcinoma. Whether glucose autoregulates its own metabolism remains poorly understood. To probe this, we performed RNA-Seq analysis on MCF7 breast cancer cells cultured with/without short-term glucose withdrawal.

2023-06-29 | GSE206393 | GEO

Effect of short-term glucose withdrawal on gene expression of MCF7 cells

Project description:Effect of short-term glucose withdrawal on gene expression of MCF7 cells

| PRJNA850428 | ENA

Effect of short-term glucose withdrawal and glucose refeeding after short-term glucose withdrawal on gene expression of MCF7 cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-29 | GSE206396 | GEO

Stress responses elicited by glucose withdrawal in Aspergillus fumigatus

Project description:Glucose is a widely used carbon source in laboratory practice to culture Aspergillus fumigatus, however, glucose availability is often low in its “natural habitats” including the human body. We used a physiological–transcriptomical approach to reveal differences between A. fumigatus Af293 cultures incubated on glucose, glucose and peptone, peptone (carbon limitation), or without any carbon source (carbon starvation). Autolytic cell wall degradation was upregulated by both carbon starvation and limitation. The importance of autolytic cell wall degradation in adaptation to carbon stress was also highlighted by approximately 12.4% of the A. fumigatus genomes harbor duplication of genes involved in N-acetyl glucosamine utilization. Glucose withdrawal increased redox imbalance, altered both the transcription of antioxidative enzyme genes and oxidative stress tolerance, downregulated iron acquisition, but upregulated heme protein genes. Transcriptional activity of the Gliotoxin cluster was low in all experiments, while the Fumagillin cluster showed substantial activity both on glucose and under carbon starvation, and the Hexadehydro-astechrome cluster only on glucose. We concluded that glucose withdrawal substantially modified the physiology of A. fumigatus including processes that contribute to virulence. This may explain the challenge of predicting the in vivo behavior of A. fumigatus based on data from glucose rich cultures.

2022-12-09 | GSE216000 | GEO

Stress responses elicited by glucose withdrawal in Aspergillus fumigatus

Project description:Stress responses elicited by glucose withdrawal in Aspergillus fumigatus

| PRJNA891691 | ENA

Transcription profiling of human MCF7 wt and MCF7/HER2-18 xenografts

Project description:To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). Another group received ED plus the antiestrogen fulvestrant (MCF7 wt only). Tumors with acquired or de novo resistance to these endocrine therapies were profiled for mRNA expression using Affymetrix Genechip arrays. This SuperSeries is composed of the following subset Series:; GSE8139: Expression data from MCF7/HER2-18 xenografts; GSE8140: Expression data from MCF7 wt xenografts Experiment Overall Design: MCF7 xenografts were established in ovariectomized five to six week-old nu/nu athymic nude mice supplemented with 0.25 mg 21 day release estrogen pellets by inoculating subcutaneously (s.c.) 5E-6 cells. When tumors reached the size of 150-200 mm3 (3-5 weeks), the animals were randomly allocated to continued estrogen (E2), continued estrogen with gefitinib (E2+G; 100mg/kg, 5 days/week), estrogen withdrawal alone (ED; by removal of the estrogen pellets), and estrogen withdrawal plus tamoxifen citrate (Tam; 500 microg/animal s.c. in peanut oil, 5 days/week), with either gefitinib (Tam+G; 100mg/kg, 5 days/week) or vehicle (1% Tween 80) administered via gavage, as well as estrogen withdrawal plus fulvestrant (ICI 182,780) in the MCF7 wt model (Fulv; 5mg/mouse s.c. once weekly), and estrogen withdrawal with gefitinib (ED+G). Tumors were harvested for molecular studies when they became resistant to treatment and reached the size of 1000 mm3 (n=7). Experiment Overall Design: Refer to individual Series

2008-12-05 | E-GEOD-8141 | biostudies-arrayexpress

Transcription profiling of mouse MCF7 wt xenografts

Project description:To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). Another group received ED plus the antiestrogen fulvestrant (MCF7 wt only). Tumors with acquired or de novo resistance to these endocrine therapies were profiled for mRNA expression using Affymetrix Genechip arrays. Experiment Overall Design: MCF7 xenografts were established in ovariectomized five to six week-old nu/nu athymic nude mice supplemented with 0.25 mg 21 day release estrogen pellets by inoculating subcutaneously (s.c.) 5E-6 cells. When tumors reached the size of 150-200 mm3 (3-5 weeks), the animals were randomly allocated to continued estrogen (E2), continued estrogen with gefitinib (E2+G; 100mg/kg, 5 days/week), estrogen withdrawal alone (ED; by removal of the estrogen pellets), and estrogen withdrawal plus tamoxifen citrate (Tam; 500 microg/animal s.c. in peanut oil, 5 days/week), with either gefitinib (Tam+G; 100mg/kg, 5 days/week) or vehicle (1% Tween 80) administered via gavage, as well as estrogen withdrawal plus fulvestrant (ICI 182,780) in the MCF7 wt model (Fulv; 5mg/mouse s.c. once weekly), and estrogen withdrawal with gefitinib (ED+G). Tumors were harvested for molecular studies when they became resistant to treatment and reached the size of 1000 mm3 (n=7).

2009-01-13 | E-GEOD-8140 | biostudies-arrayexpress

Short term perturbation

Project description:Study of the short term (within the first 330 seconds) transcriptional response of S.cerevisiae upon a sudden addition of glucose. Keywords: glucose pulse, chemostat culture, glucose catabolite repression

2005-12-16 | GSE3821 | GEO

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