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Selective advantage of epigenetically disrupted cancer cells via phenotypic inertia [scRNA-seq]

ABSTRACT: Identification of gene expression changes at the single-cell level induced by glutamine deprivation in melanoma cells lacking various epigenetic regulators

ORGANISM(S): Homo sapiens

PROVIDER: GSE178641 | GEO | 2022/11/03

REPOSITORIES: GEO

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Selective advantage of epigenetically disrupted cancer cells via phenotypic inertia [RNA-seq]

Project description:Identification of gene expression changes induced by glutamine deprivation in melanoma cells lacking various epigenetic regulators

2022-11-03 | GSE178306 | GEO

Selective advantage of epigenetically disrupted cancer cells via phenotypic inertia [ATAC-Seq]

Project description:Mutations in over one hundred genes, belonging to diverse classes of epigenetic regulators, resulted in significant fitness advantage under nutrient starvation and acidic conditions, suggesting that disruption of epigenetic control, at multiple levels of the regulatory network, promotes broad resistance of cells to stressful environments. To uncover the molecular mechanisms of such phenomenon, and to understand how loss of epigenetic regulators gives advantage during stress, we examined how chromatin accessibility changes in nutrient-deprived conditions using ATAC-seq. ATAC-seq analysis of melanoma cells expressing 4-7sgRNAs targeting members of the PRC2 complex (EED, EZH2, SUZ12), histone H1B (HIST1H1B), the chromatin remodeller SMARCD1 and a non-expressed control gene (TNP2), and grown in either unperturbed conditions (d0) or under glutamine deprivation (d2).

2022-11-03 | GSE212744 | GEO

Selective advantage of epigenetically disrupted cancer cells via phenotypic inertia [Exome-seq]

Project description:Aim: assess the contribution of de-novo clonal mutations to the observed adaptive behaviours to nutrient starvation in PDX derived melanoma and lung cancer cells. Methods: Identical replicates from both cancer models were plated in 96 wells plates and grown in starvation (RPMI media lacking L-glutamine). After prolonged exposure to starvation, extensive phenotypic variability was observed. We selected populations that managed to adapt (t20 samples, strong but also moderate phenotypes) and performed exome-seq. Comparison of their mutational landscape with the initial parental populations (t=0) will uncover possible candidates that drive the adaptation of these populations. Results: Absence of any selected clonal mutation within individual resistant populations or recurrent subclonal mutations across replicates Conclusions: The stochastic adaptive behaviours observed upon starvation in PDX MeA5a and L1C5c derived lines does not seem to be confered through selection of clonal genetic events.

2022-11-03 | GSE178642 | GEO

Selective advantage of epigenetically disrupted cancer cells via phenotypic inertia

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

2022-11-03 | GSE178643 | GEO

Selective advantage of epigenetically disrupted cancer cells via phenotypic inertia [ChIP-Seq]

2022-11-03 | GSE212693 | GEO

Dietary glutamine supplementation suppresses epigenetically-activated oncogenic pathways to inhibit melanoma tumour growth

Project description:Tumour cells adapt to nutrient deprivation in vivo, yet strategies targeting the nutrient poor microenvironment remain unexplored. We recently found, in melanoma, tumour cells often experience low glutamine levels, which induce histone hypermethylation, promote dedifferentiation, and increase resistance to BRAF inhibitors. These findings raise the possibility that increased glutamine levels can be detrimental to melanoma tumours. Here, we show that dietary glutamine supplementation significantly inhibits melanoma tumour growth, prolongs survival in transgenic mouse model, and increases sensitivity to BRAF targeted inhibitors in both melanoma xenograft and patient-derived xenograft (PDX) models. Notably, metabolomic analysis reveals that dietary uptake of glutamine effectively increases the concentration of glutamine and its downstream metabolite, αKG, in serum and tumours, without increasing biosynthetic intermediates necessary for cell proliferation. Mechanistically, we find that glutamine supplementation uniformly alters the transcriptome and suppresses expression of many melanoma-associated genes. Our data further demonstrate that increase in intra-tumoural αKG concentration, following glutamine supplementation, drives hypomethylation of H3K4me3, thereby suppressing epigenetically-activated oncogenic pathways in melanoma. Therefore, our findings provide important evidence that glutamine supplementation can serve as a potential dietary intervention to block melanoma tumour growth and sensitize tumours to targeted therapy via epigenetic reprogramming.

2020-05-14 | GSE140274 | GEO

Glutamine deprivation in U2OS cells

2014-07-31 | GSE59931 | GEO

Glutamine deprivation in U2OS cells

Project description:To understand the effects of glutamine deprivation on cell physiology we performed global analysis of gene expression in response to glutamine deprivation. U2OS cells were subjected to glutamine deprivation for 24h followed by RNA extraction and microarray analysis. U2OS cells were plated overnight followed by treatment for 24h with glutamine-containing and glutamine-depleted media. Three biological replicates were assayed for each condition.

2014-07-31 | E-GEOD-59931 | biostudies-arrayexpress

Homo sapiens

Project description:Glutamine deprivation in U2OS cells

| PRJNA257073 | ENA

Proteomic analysis of glutamine deprivation in HepG2 cells

Project description:We applied the quantitative proteomics approach to estimate the relative abundance of proteins in HepG2 cells treated by glutamine deprivation. Two independent cultured cell lysates, namely control and glutamine deprivation, were marked with iTRAQ labels and subjected to LC-ESI-MS/MS analysis. The tryptic peptides of two samples were labeled with mass 113 (control) and 119 (glutamine deprivation) isobaric iTRAQ tags.

2017-03-29 | MSV000080721 | MassIVE

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