ArticleMolecular biology of the cell2016
Transcriptome analysis of tetraploid cells identifies cyclin D2 as a facilitator of adaptation to genome doubling in the presence of p53.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 63 citations in OpenAlex.
- Atypical fusion among non-malignant cells: Unveiling the link between post-fusion-induced genome chaos and cancer initiation.Cancer cell international · 2026Article
- Power-law scaling of mitotic spindles with genome sizes across eukaryotes is driven by chromosome crowding.Nature cell biology · 2026Article
- Lamin B1-dependent regulation of human separase in mitosis.Nucleic acids research · 2026Article
- Tetraploids or polyploid giants: who is truly dangerous?Trends in cell biology · 2026Review
- Profiling cell proliferation after whole-genome duplication in human cells.Biology open · 2026Article
- Cell and Nuclear Size Is Associated with Chromosomal Instability and Tumorigenicity in Cancer Cells That Undergo Whole Genome Doubling.Cancer research · 2026Article
- Sister chromatid separation determines the proliferative properties upon whole-genome duplication via homologous chromosome arrangement.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Genomic Reshuffling After Cell Fusion: Catalyst for Cancer Evolution and Progression.Advances in experimental medicine and biology · 2026Review
- M phase-specific generation of supernumerary centrioles in cancer cells.Molecular biology of the cell · 2025Article
- Anillin Recedes in p53-Dependent Senescence of Tumor Cells and Reappears in Cells Escaping from Senescence.Aging and disease · 2025Article
- Review
- Proteogenomic analysis reveals adaptive strategies for alleviating the consequences of aneuploidy in cancer.The EMBO journal · 2025Article
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- Polyploids broadly generate novel haplotypes from trans-specific variation in Arabidopsis arenosa and Arabidopsis lyrata.PLoS genetics · 2024Article
- Surviving the Storm: The Role of Poly- and Depolyploidization in Tissues and Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.Journal of experimental & clinical cancer research : CR · 2024Article
- Whole-genome doubling in tissues and tumors.Trends in genetics : TIG · 2023Review
- Permission to pass: on the role of p53 as a gatekeeper for aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- Computational Biology Helps Understand How Polyploid Giant Cancer Cells Drive Tumor Success.Genes · 2023Review
- Whole-Genome Duplication and Genome Instability in Cancer Cells: Double the Trouble.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Tetraploidization, or genome doubling, is a prominent event in tumorigenesis, primarily because cell division in polyploid cells is error-prone and produces aneuploid cells. This study investigates changes in gene expression evoked in acute and adapted tetraploid cells and their effect on cell-cycle progression. Acute polyploidy was generated by knockdown of the essential regulator of cytokinesis anillin, which resulted in cytokinesis failure and formation of binucleate cells, or by chemical inhibition of Aurora kinases, causing abnormal mitotic exit with formation of single cells with aberrant nuclear morphology. Transcriptome analysis of these acute tetraploid cells revealed common signatures of activation of the tumor-suppressor protein p53. Suppression of proliferation in these cells was dependent on p53 and its transcriptional target, CDK inhibitor p21. Rare proliferating tetraploid cells can emerge from acute polyploid populations. Gene expression analysis of single cell-derived, adapted tetraploid clones showed up-regulation of several p53 target genes and cyclin D2, the activator of CDK4/6/2. Overexpression of cyclin D2 in diploid cells strongly potentiated the ability to proliferate with increased DNA content despite the presence of functional p53. These results indicate that p53-mediated suppression of proliferation of polyploid cells can be averted by increased levels of oncogenes such as cyclin D2, elucidating a possible route for tetraploidy-mediated genomic instability in carcinogenesis.
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