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Selective advantage of epigenetically disrupted cancer cells via phenotypic inertia

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE178643 | GEO | 2022/11/03

REPOSITORIES: GEO

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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.

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

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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).

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Selective advantage of epigenetically disrupted cancer cells via phenotypic inertia

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

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