Effect of glucose refeeding after short-term glucose withdrawal on gene expression of MCF7 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE206394 | GEO | 2023/06/29
REPOSITORIES: GEO
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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
Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:The discovery of FoxO1 as an effector of insulin action on gene expression filled a gap in our knowledge of insulin signaling. The metabolic impact of hepatic FoxO1 has been demonstrated in genetic mouse models showing that FoxO1 inhibition can reverse diabetes. However, the gamut of FoxO1 targets is unknown, due to the lack of robust genome-wide chromatin occupancy data. To elucidate the genomic architecture of the FoxO1 effect on liver metabolism, we integrated genome-wide ChIP-seq and RNA-seq. During the physiological transition from fasting to refeeding, hepatic FoxO1 translocated from the nucleus to the cytoplasm. At the same time points, cistrome analysis demonstrated that 60% of FoxO1 target sites were cleared by refeeding. RNA-seq from mice following acute liver-specific FoxO1 ablation allowed us to integrate the data in a comprehensive FoxO1 regulome. We identified four distinct classes of FoxO1 targets. Class I targets are enriched in genes regulating cell homeostasis, have FoxO1 sites clustered in promoters and do not show regulation with fasting/refeeding. Class II is comprised of canonical FoxO1 metabolic targets coordinately regulated with other fasting-inducible TFs, such as PPARA, CREB, and GR through promoters. Class III is enriched in glucose metabolic genes regulated through active enhancers, as detected by H3K4me1 and H3K27ac histone marks. Class IV is comprised of triglyceride (TG) and lipoprotein metabolism genes, regulated through intron sites, and characterized by an uneven response to fasting/refeeding regulation.
2022-05-24 | GSE151545 | GEO
Project description:The discovery of FoxO1 as an effector of insulin action on gene expression filled a gap in our knowledge of insulin signaling. The metabolic impact of hepatic FoxO1 has been demonstrated in genetic mouse models showing that FoxO1 inhibition can reverse diabetes. However, the gamut of FoxO1 targets is unknown, due to the lack of robust genome-wide chromatin occupancy data. To elucidate the genomic architecture of the FoxO1 effect on liver metabolism, we integrated genome-wide ChIP-seq and RNA-seq. During the physiological transition from fasting to refeeding, hepatic FoxO1 translocated from the nucleus to the cytoplasm. At the same time points, cistrome analysis demonstrated that 60% of FoxO1 target sites were cleared by refeeding. RNA-seq from mice following acute liver-specific FoxO1 ablation allowed us to integrate the data in a comprehensive FoxO1 regulome. We identified four distinct classes of FoxO1 targets. Class I targets are enriched in genes regulating cell homeostasis, have FoxO1 sites clustered in promoters and do not show regulation with fasting/refeeding. Class II is comprised of canonical FoxO1 metabolic targets coordinately regulated with other fasting-inducible TFs, such as PPARA, CREB, and GR through promoters. Class III is enriched in glucose metabolic genes regulated through active enhancers, as detected by H3K4me1 and H3K27ac histone marks. Class IV is comprised of triglyceride (TG) and lipoprotein metabolism genes, regulated through intron sites, and characterized by an uneven response to fasting/refeeding regulation.
2022-05-24 | GSE151544 | GEO
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.
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Project description:We report the single-cell RNA sequencing data obtained from MCF7 breast cancer cells cultured in standard DMEM with 25 mM glucose, or adapted to culture in DMEM with 10 mM fructose to reduce glycolysis, and cultures in 2D on plastic
2020-05-28 | GSE115869 | GEO
Project description:In this RNA-Seq dataset, we describe transcriptomic changes in whole dissected intestinal tracts taken from adult zebrafish that were either fed normally or subjected to a prolonged starvation/refeeding regimen. Analysis of this RNA-Seq data revealed starvation-induced alterations in transcript levels for many genes, including a decrease in lipid metabolism and an increase in innate immune responses. Refeeding for as little as 3 days after starvation was sufficient to restore most transcripts to their baseline pre-starvation levels. These host RNA-Seq results are accompanied by a 16S rRNA gene sequencing dataset from similarly treated adult zebrafish to define changes in intestinal microbiome composition associated with starvation and refeeding.
2021-01-31 | GSE140821 | GEO
Project description:Metabolic diseases, including type 2 diabetes and obesity are relevant negative prognostic factor in patients with breast cancer (BC). We have investigated the mechanisms through which elevated glucose levels affect tamoxifen sensitivity of estrogen receptor positive (ER+) BC cells. We found that MCF7 BC cell sensitivity to tamoxifen was 2-fold reduced in 25mM glucose (HG), a concentration mimicking hyperglycaemia, compared to 5.5 mM glucose (LG), resembling normal fasting glucose levels in humans. Shifting MCF7 cells from HG to LG ameliorated their responsiveness to tamoxifen. RNA-Sequencing revealed that glucose modified the transcriptome of MCF7 cells. In particular, cell cycle-related genes were affected by glucose. Combining gene specific knockdown and treatment with human recombinant proteins, we identified the Connective Tissue Growth Factor (CTGF) as glucose-induced factor able to reduce MCF7 cell sensitivity to tamoxifen. Moreover, we found that both CTGF expression levels and tamoxifen responsiveness were enhanced co-culturing MCF7 cells with human adipocytes through an Interleukin-8 (IL8)-mediated mechanism. Indeed, IL8 inhibition reduced CTGF levels and rescued tamoxifen sensitivity in MCF7 cells. Interestingly, CTGF immuno-detection in bioptic specimens obtained from women with ER+ BC correlated with distant metastases (P-value = 0.000), hormone therapy resistance (P-value = 0.000), reduced overall (P-value = 0.051) and disease free survival (P-value = 0.000). Thus, glucose affects tamoxifen responsiveness directly modulating CTGF in BC cells, and indirectly promoting the adipocytes’ release of IL8. Both CTGF and IL8 may represent potential targets in novel therapeutic strategies to increase tamoxifen sensitivity.
2017-07-01 | GSE97647 | GEO
Project description:For more than a century, fasting regimens have been shown to improve health, lifespan, and tissue regeneration in diverse model organisms and humans. However, important questions remain regarding how fasting and refeeding cycles stimulate stem cell output and how this influences their role in early tumor formation. Here, we demonstrate that in the mammalian intestine, a short 24-hour fast followed by a 24-hour refeeding period (that is, post-fast refeeding) and not fasting itself elevates the stemness program and regenerative capacity of Lgr5+ intestinal stem cells (ISCs). Furthermore, loss of the tumor suppressor APC in post-fast refed ISCs significantly boosts tumor incidence in the small intestine and colon compared to those in the fasted or ad libitum fed states. Mechanistically, robust induction of insulin-PI3K-mTORC1 signaling as well as elevated intestinal polyamines level increase protein synthesis in post-fast refed ISCs to mediate these changes as inhibition of mTORC1, polyamine, or protein synthesis abrogate the regenerative or tumorigenic effects of post-fast refeeding. Thus, our data indicate that post-fast refeeding leads to a burst not only in stem cell-driven regeneration but also in tumorigenicity and that careful consideration be given to fast-refeeding cycles when planning diet-based strategies.
2023-08-08 | GSE192482 | GEO