Epigenetic reprogramming of melanoma cells by vitamin C treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE121095 | GEO | 2018/10/10
REPOSITORIES: GEO
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Project description:In this study we show that ascorbate (vitamin C) shifts the transcriptome of MDA-MB-231 cells and increases apoptosis.
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Project description:Ascorbate (vitamin C) is an essential micronutrient in humans. The chronic severe deficiency of ascorbate, termed scurvy, has long been associated with increased susceptibility to infections. How ascorbate affects the immune system at the cellular and molecular levels remained unclear. Here, from a micronutrient screen, we identified ascorbate as a potent enhancer for antibody response by facilitating the IL-21/STAT3-dependent plasma cell differentiation in mouse and human B cells. The effect of ascorbate is unique, as other antioxidants failed to promote plasma cell differentiation. Ascorbate is critical during early B cell activation by poising the cells to plasma cell lineage without affecting the proximal IL-21/STAT3 signaling and the overall transcriptome. Consistent with its role as a cofactor for epigenetic enzymes, ascorbate potentiates plasma cell differentiation by remodeling the epigenome via TET (Ten Eleven Translocation), the enzymes responsible for DNA demethylation by oxidizing 5-methylcytosines into 5-hydroxymethylcytosine (5hmC). Genomewide 5hmC profiling identified ascorbate responsive elements (EAR) at the Prdm1 locus, including a distal element with a STAT3 motif overlapped with a CpG that was methylated and modified by TET in the presence of ascorbate. The results suggest that an adequate level of VC is required for antibody response and highlight how micronutrients can cooperate with epigenetic enzymes to regulate gene expression. Our finding also implies that epigenetic enzymes can function as sensors to gauge the availability of metabolites and influence cell fate decisions.
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Project description:Ascorbate (vitamin C) is an essential micronutrient in humans. The chronic severe deficiency of ascorbate, termed scurvy, has long been associated with increased susceptibility to infections. How ascorbate affects the immune system at the cellular and molecular levels remained unclear. Here, from a micronutrient screen, we identified ascorbate as a potent enhancer for antibody response by facilitating the IL-21/STAT3-dependent plasma cell differentiation in mouse and human B cells. The effect of ascorbate is unique, as other antioxidants failed to promote plasma cell differentiation. Ascorbate is critical during early B cell activation by poising the cells to plasma cell lineage without affecting the proximal IL-21/STAT3 signaling and the overall transcriptome. Consistent with its role as a cofactor for epigenetic enzymes, ascorbate potentiates plasma cell differentiation by remodeling the epigenome via TET (Ten Eleven Translocation), the enzymes responsible for DNA demethylation by oxidizing 5-methylcytosines into 5-hydroxymethylcytosine (5hmC). Genomewide 5hmC profiling identified ascorbate responsive elements (EAR) at the Prdm1 locus, including a distal element with a STAT3 motif overlapped with a CpG that was methylated and modified by TET in the presence of ascorbate. The results suggest that an adequate level of VC is required for antibody response and highlight how micronutrients can cooperate with epigenetic enzymes to regulate gene expression. Our finding also implies that epigenetic enzymes can function as sensors to gauge the availability of metabolites and influence cell fate decisions.
2022-09-06 | GSE183680 | GEO
Project description:Ascorbate (vitamin C) is an essential micronutrient in humans. The chronic severe deficiency of ascorbate, termed scurvy, has long been associated with increased susceptibility to infections. How ascorbate affects the immune system at the cellular and molecular levels remained unclear. Here, from a micronutrient screen, we identified ascorbate as a potent enhancer for antibody response by facilitating the IL-21/STAT3-dependent plasma cell differentiation in mouse and human B cells. The effect of ascorbate is unique, as other antioxidants failed to promote plasma cell differentiation. Ascorbate is critical during early B cell activation by poising the cells to plasma cell lineage without affecting the proximal IL-21/STAT3 signaling and the overall transcriptome. Consistent with its role as a cofactor for epigenetic enzymes, ascorbate potentiates plasma cell differentiation by remodeling the epigenome via TET (Ten Eleven Translocation), the enzymes responsible for DNA demethylation by oxidizing 5-methylcytosines into 5-hydroxymethylcytosine (5hmC). Genomewide 5hmC profiling identified ascorbate responsive elements (EAR) at the Prdm1 locus, including a distal element with a STAT3 motif overlapped with a CpG that was methylated and modified by TET in the presence of ascorbate. The results suggest that an adequate level of VC is required for antibody response and highlight how micronutrients can cooperate with epigenetic enzymes to regulate gene expression. Our finding also implies that epigenetic enzymes can function as sensors to gauge the availability of metabolites and influence cell fate decisions.
2022-09-06 | GSE206453 | GEO
Project description:Ascorbate (vitamin C) is an essential micronutrient in humans. The chronic severe deficiency of ascorbate, termed scurvy, has long been associated with increased susceptibility to infections. How ascorbate affects the immune system at the cellular and molecular levels remained unclear. Here, from a micronutrient screen, we identified ascorbate as a potent enhancer for antibody response by facilitating the IL-21/STAT3-dependent plasma cell differentiation in mouse and human B cells. The effect of ascorbate is unique, as other antioxidants failed to promote plasma cell differentiation. Ascorbate is critical during early B cell activation by poising the cells to plasma cell lineage without affecting the proximal IL-21/STAT3 signaling and the overall transcriptome. Consistent with its role as a cofactor for epigenetic enzymes, ascorbate potentiates plasma cell differentiation by remodeling the epigenome via TET (Ten Eleven Translocation), the enzymes responsible for DNA demethylation by oxidizing 5-methylcytosines into 5-hydroxymethylcytosine (5hmC). Genomewide 5hmC profiling identified ascorbate responsive elements (EAR) at the Prdm1 locus, including a distal element with a STAT3 motif overlapped with a CpG that was methylated and modified by TET in the presence of ascorbate. The results suggest that an adequate level of VC is required for antibody response and highlight how micronutrients can cooperate with epigenetic enzymes to regulate gene expression. Our finding also implies that epigenetic enzymes can function as sensors to gauge the availability of metabolites and influence cell fate decisions.
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Project description:: In the present study, we used the Gulo-/- female and male mice model which depends entirely on ascorbate derived from the diet. We tested different concentrations of ascorbate ranging from 0 to 0.4% (w/v) ascorbate, added into drinking water, until the age of four months. Importantly, the levels of ascorbate found in the liver of Gulo-/- mice reflect the amounts of ascorbate provided in drinking water. We performed label-free Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) global quantitative proteomic profiling to identify and quantify proteins in whole liver extracts from our different ascorbate treated cohorts of Gulo-/- females and males. We compared the proteomic profiles to the transcriptomic profiles of the same treated animals. Although several proteins of the mitochondrial complex III significantly correlated with vitamin C concentrations, their corresponding transcripts did not correlate with vitamin C in both females and males. Such observations were confirmed by western blot and quantitative RT-PCR analyses, respectively. Our findings suggest that transcriptome profiling alone provides an incomplete picture of molecular changes associated with vitamin C deficiency in the liver of mice and examination of changes in protein abundances is essential to unveil variations that are not transcriptionally regulated.
2023-05-26 | MSV000092040 | MassIVE
Project description:Vitamin C (ascorbate) is a crucial antioxidant and an essential cofactor of biosynthetic and regulatory enzymes. Unlike humans, mice can synthesize vitamin C thanks to the key enzyme gulonolactone oxidase (Gulo). In the present study, we used the Gulo-/- mouse model, which cannot synthesize their own ascorbate to determine the impact of this vitamin on both the transcriptomics and proteomics profiles in the liver. The study included Gulo-/- mouse groups treated with either sub-optimal or optimal vitamin C concentrations in drinking water. We found a distinctive difference in the mRNA and protein profiles as a function of sex between all the mouse groups. Despite this sexual dimorphism, Spearman correlation analyses were conducted to divulge which transcripts and proteins correlated with hepatic vitamin C concentrations in both females and males. Such analysis on transcriptomics data from females and males revealed changes in a wide array of biological processes involved in glucose, lipid, steroid, and glutathione metabolisms as well as in acute-phase response. Furthermore, although several proteins of the mitochondrial complex III significantly correlated with vitamin C concentrations, their corresponding transcripts did not correlate with vitamin C in both females and males. Thus, this side-by-side comparison between transcriptome and proteome supported the view that post-transcriptional processes play a major role in the regulation of cellular respiration in the liver upon vitamin C deficiency. Our findings suggest that transcriptome profiling alone provides an incomplete picture of molecular changes associated with vitamin C deficiency in the liver of mice and examination of changes in protein abundances is essential to unveil variations that are not transcriptionally regulated.
2023-06-01 | GSE233598 | GEO