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The deregulated microRNAome contributes to the cellular response to aneuploidy [miRNA]

ABSTRACT: Aneuploidy severely alters cell physiology and is widespread in cancers and other pathologies. In model cell lines, aneuploidy impairs proliferation, leads to proteotoxic as well as replication stress and triggers conserved transcriptome and proteome changes. In this study we analysed for the first time miRNAs and demonstrate that their expression is altered in response to chromosome gain.

ORGANISM(S): Homo sapiens

PROVIDER: GSE102854 | GEO | 2018/02/09

REPOSITORIES: GEO

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The deregulated microRNAome contributes to the cellular response to aneuploidy [mRNA]

Project description:Aneuploidy severely alters cell physiology and is widespread in cancers and other pathologies. In model cell lines, aneuploidy impairs proliferation, leads to proteotoxic as well as replication stress and triggers conserved transcriptome and proteome changes. In this study we analysed for the first time miRNAs and demonstrate that their expression is altered in response to chromosome gain.

2018-02-09 | GSE102852 | GEO

The deregulated microRNAome contributes to the cellular response to aneuploidy.

Project description:BackgroundAneuploidy, or abnormal chromosome numbers, severely alters cell physiology and is widespread in cancers and other pathologies. Using model cell lines engineered to carry one or more extra chromosomes, it has been demonstrated that aneuploidy per se impairs proliferation, leads to proteotoxic as well as replication stress and triggers conserved transcriptome and proteome changes.ResultsIn this study, we analysed for the first time miRNAs and demonstrate that their expression is altered in response to chromosome gain. The miRNA deregulation is independent of the identity of the extra chromosome and specific to individual cell lines. By cross-omics analysis we demonstrate that although the deregulated miRNAs differ among individual aneuploid cell lines, their known targets are predominantly associated with cell development, growth and proliferation, pathways known to be inhibited in response to chromosome gain. Indeed, we show that up to 72% of these targets are downregulated and the associated miRNAs are overexpressed in aneuploid cells, suggesting that the miRNA changes contribute to the global transcription changes triggered by aneuploidy. We identified hsa-miR-10a-5p to be overexpressed in majority of aneuploid cells. Hsa-miR-10a-5p enhances translation of a subset of mRNAs that contain so called 5'TOP motif and we show that its upregulation in aneuploids provides resistance to starvation-induced shut down of ribosomal protein translation.ConclusionsOur work suggests that the changes of the microRNAome contribute on one hand to the adverse effects of aneuploidy on cell physiology, and on the other hand to the adaptation to aneuploidy by supporting translation under adverse conditions.

| S-EPMC6389165 | biostudies-literature

The deregulated microRNAome contributes to the cellular response to aneuploidy

Project description:The deregulated microRNAome contributes to the cellular response to aneuploidy

| PRJNA399120 | ENA

The deregulated microRNAome contributes to the cellular response to aneuploidy

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

2018-02-09 | GSE102855 | GEO

Four layer multi-omics reveals molecular responses to aneuploidy in Leishmania

Project description:Aneuploidy causes system-wide disruptions in the stochiometric balances of transcripts, proteins, and metabolites, often resulting in detrimental effects for the organism. The protozoan parasite Leishmania has an unusually high tolerance for aneuploidy, but the molecular and functional consequences for the pathogen remain poorly understood. Here, we addressed this question in vitro and present the first integrated analysis of the genome, transcriptome, proteome, and metabolome of highly aneuploid Leishmania donovani strains. Our analyses unambiguously establish that aneuploidy in Leishmania proportionally impacts the average transcript- and protein abundance levels of affected chromosomes, ultimately correlating with the degree of metabolic differences between strains. This proportionality was present in both proliferative and non-proliferative in vitro promastigotes. However, protein complex subunits and non-cytoplasmic proteins, showed dosage compensation, responding less or even not at all to aneuploidy-induced dosage changes. In contrast to other Eukaryotes, we did not observe the widespread regulation at the transcript level that typically modulates some of the negative effects of aneuploidy. Further, the majority of differentially expressed proteins between aneuploid strains were encoded by non-aneuploid chromosomes and were not driven by a significant underlying transcript change, suggesting that aneuploidy is accompanied by extensive post-transcriptional protein-level modulation. This makes Leishmania a unique Eukaryotic model for elucidating post-transcriptional protein-abundance modulation in the context of aneuploidy. Data availability:Proteomic data associated with this study are available in the PRIDE repository: accession number <a href='https://www.ebi.ac.uk/pride/archive/projects/PXD028521' rel='noopener noreferrer' target='_blank'>PXD028521</a>.

2022-09-19 | MTBLS1612 | MetaboLights

Mosaic Chromosomal Aneuploidy

Project description:Mosaic Chromosomal Aneuploidy

| PRJNA437525 | ENA

Mosaic Chromosomal Aneuploidy

Project description:Mosaic Chromosomal Aneuploidy

| PRJNA437526 | ENA

Aneuploidy

Project description:Aneuploidy promotes genomic instability by impairing DNA replication

| PRJEB7596 | ENA

Quantitative Proteomic Analysis Reveals Posttranslational Responses to Aneuploidy in Yeast

Project description:Aneuploidy causes severe developmental defects and is a near universal feature of tumor cells. Despite its profound effects, the cellular processes affected by aneuploidy are not well characterized. Here, we examined the consequences of aneuploidy on the proteome of aneuploid budding yeast strains. We show that although protein levels largely scale with gene copy number, subunits of multi-protein complexes are notable exceptions. Posttranslational mechanisms attenuate their expression when their encoding genes are in excess. Our proteomic analyses further revealed a novel aneuploidy-associated protein expression signature characteristic of altered metabolism and redox homeostasis. Indeed aneuploid cells harbor increased levels of reactive oxygen species (ROS). Interestingly, increased protein turnover attenuates ROS levels and this novel aneuploidy-associated signature and improves the fitness of most aneuploid strains. Our results show that aneuploidy causes alterations in metabolism and redox homeostasis. Cells respond to these alterations through both transcriptional and posttranscriptional mechanisms.

2014-08-14 | PXD001019 | Pride

Consequences of aneuploidy in human fibroblasts

Project description:To characterize aneuploidy driven phenotypes in human trisomies, we performed global transcriptome, proteome, and phenotypic analysis of primary human fibroblasts from individuals with Patau (trisomy 13), Edwards (trisomy 18), or Down syndromes.

2020-07-09 | MSV000085706 | MassIVE

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