ArticleeLife2022
Regulation of protein complex partners as a compensatory mechanism in aneuploid tumors.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- NAC promotes co-translational protein folding at the ribosomal tunnel exit.Molecular cell · 2026Article
- Energetics of whole genome doubling and genomic instability.Cancer letters · 2025Review
- Proteomic compensation by paralogs preserves protein interaction networks after gene loss in cancer.Molecular systems biology · 2025Article
- Multilevel Gene Expression Changes in Lineages Containing Adaptive Copy Number Variants.Molecular biology and evolution · 2025Article
- Increased RNA and Protein Degradation Is Required for Counteracting Transcriptional Burden and Proteotoxic Stress in Human Aneuploid Cells.Cancer discovery · 2024Article
- Reduction of chromosomal instability and inflammation is a common aspect of adaptation to aneuploidy.EMBO reports · 2024Article
- Multilevel gene expression changes in lineages containing adaptive copy number variants.bioRxiv : the preprint server for biology · 2024Article
- Article
- Gene dosage compensation: Origins, criteria to identify compensated genes, and mechanisms including sensor loops as an emerging systems-level property in cancer.Cancer medicine · 2023Review
- Compromised Mitotic Fidelity in Human Pluripotent Stem Cells.International journal of molecular sciences · 2023Review
- Cancer genomes tolerate deleterious coding mutations through somatic copy number amplifications of wild-type regions.Nature communications · 2023Article
- The permissive binding theory of cancer.Frontiers in oncology · 2023Article
- Extensive protein dosage compensation in aneuploid human cancers.Genome research · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aneuploidy, a state of chromosome imbalance, is a hallmark of human tumors, but its role in cancer still remains to be fully elucidated. To understand the consequences of whole-chromosome-level aneuploidies on the proteome, we integrated aneuploidy, transcriptomic, and proteomic data from hundreds of The Cancer Genome Atlas/Clinical Proteomic Tumor Analysis Consortium tumor samples. We found a surprisingly large number of expression changes happened on other, non-aneuploid chromosomes. Moreover, we identified an association between those changes and co-complex members of proteins from aneuploid chromosomes. This co-abundance association is tightly regulated for aggregation-prone aneuploid proteins and those involved in a smaller number of complexes. On the other hand, we observed that complexes of the cellular core machinery are under functional selection to maintain their stoichiometric balance in aneuploid tumors. Ultimately, we provide evidence that those compensatory and functional maintenance mechanisms are established through post-translational control, and that the degree of success of a tumor to deal with aneuploidy-induced stoichiometric imbalance impacts the activation of cellular protein degradation programs and patient survival.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.