ArticleMolecular biology of the cell2018
Quantitative proteomic and phosphoproteomic comparison of human colon cancer DLD-1 cells differing in ploidy and chromosome stability.
Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
- Protein buffering of aneuploidy is driven by coordinated factors identified through machine learning.Molecular systems biology · 2026Article
- Transcriptomic Landscape of Paclitaxel-Induced Multidrug Resistance in 3D Cultures of Colon Cancer Cell Line DLD1.International journal of molecular sciences · 2025Article
- Aneuploidy-induced proteostasis disruption impairs mitochondrial functions and mediates aggregation of mitochondrial precursor proteins through SQSTM1/p62.Nature communications · 2025Article
- Proteogenomic analysis reveals adaptive strategies for alleviating the consequences of aneuploidy in cancer.The EMBO journal · 2025Article
- Comparative Pharmacological Analysis of Mitotic Inhibitors Using Isogenic Ploidy Series of HAP1 Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Reduction of chromosomal instability and inflammation is a common aspect of adaptation to aneuploidy.EMBO reports · 2024Article
- The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024Review
- Whole-genome doubling is a double-edged sword: the heterogeneous role of whole-genome doubling in various cancer types.BMB reports · 2024Review
- Tetraploidy-linked sensitization to CENP-E inhibition in human cells.Molecular oncology · 2023Article
- A kinesin-based approach for inducing chromosome-specific mis-segregation in human cells.The EMBO journal · 2023Article
- Discovery of 2-(3-Benzamidopropanamido)thiazole-5-carboxylate Inhibitors of the Kinesin HSET (KIFC1) and the Development of Cellular Target Engagement Probes.Journal of medicinal chemistry · 2023Article
- The fate of extra centrosomes in newly formed tetraploid cells: should I stay, or should I go?Frontiers in cell and developmental biology · 2023Review
- Whole-Genome Doubling as a source of cancer: how, when, where, and why?Frontiers in cell and developmental biology · 2023Review
- Consequences of chromosome gain: A new view on trisomy syndromes.American journal of human genetics · 2022Review
- Extensive protein dosage compensation in aneuploid human cancers.Genome research · 2022Article
- Review
- Genome doubling causes double trouble.Nature · 2022Article
- Loss of USP28 and SPINT2 expression promotes cancer cell survival after whole genome doubling.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Systems approaches identify the consequences of monosomy in somatic human cells.Nature communications · 2021Article
- Chromosomal instability accelerates the evolution of resistance to anti-cancer therapies.Developmental cell · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although aneuploidy is poorly tolerated during embryogenesis, aneuploidy and whole chromosomal instability (CIN) are common hallmarks of cancer, raising the question of how cancer cells can thrive in spite of chromosome aberrations. Here we present a comprehensive and quantitative proteomics analysis of isogenic DLD-1 colorectal adenocarcinoma cells lines, aimed at identifying cellular responses to changes in ploidy and/or CIN. Specifically, we compared diploid (2N) and tetraploid (4N) cells with posttetraploid aneuploid (PTA) clones and engineered trisomic clones. Our study provides a comparative data set on the proteomes and phosphoproteomes of the above cell lines, comprising several thousand proteins and phosphopeptides. In comparison to the parental 2N line, we observed changes in proteins associated with stress responses and with interferon signaling. Although we did not detect a conspicuous protein signature associated with CIN, we observed many changes in phosphopeptides that relate to fundamental cellular processes, including mitotic progression and spindle function. Most importantly, we found that most changes detectable in PTA cells were already present in the 4N progenitor line. This suggests that activation of mitotic pathways through hyper-phosphorylation likely constitutes an important response to chromosomal burden. In line with this conclusion, cells with extensive chromosome gains showed differential sensitivity toward a number of inhibitors targeting cell cycle kinases, suggesting that the efficacy of anti-mitotic drugs may depend on the karyotype of cancer cells.
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