ArticleOncogene2004
Spindle checkpoint function is required for mitotic catastrophe induced by DNA-damaging agents.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 167 citations in OpenAlex.
- Repurposing Suan-Zao-Ren-Tang as anticancer agents in apoptotic sensitization against non-small cell lung cancer cell lines through amplification of spindle assembly checkpoint activation.Journal of traditional and complementary medicine · 2025Article
- Targeting receptor for activated C kinase 1 with a small molecule induces mitotic catastrophe and suppresses lipid metabolic reprogramming in hepatocellular carcinoma.Clinical and translational medicine · 2025Article
- Hornerin mediates phosphorylation of the polo-box domain in Plk1 by Chk1 to induce death in mitosis.Cell death and differentiation · 2023Article
- Piperine Increases Pentagamavunon-1 Anti-cancer Activity on 4T1 Breast Cancer Through Mitotic Catastrophe Mechanism and Senescence with Sharing Targeting on Mitotic Regulatory Proteins.Iranian journal of pharmaceutical research : IJPR · 2022Article
- Targeting regulated cell death (RCD) with small-molecule compounds in triple-negative breast cancer: a revisited perspective from molecular mechanisms to targeted therapies.Journal of hematology & oncology · 2022Review
- Centrosome Aberrations as Drivers of Chromosomal Instability in Breast Cancer.Endocrinology · 2021Review
- Tolerance induction in memory CD4 T cells is partial and reversible.Immunology · 2021Article
- Inhibition of the ATR kinase enhances 5-FU sensitivity independently of nonhomologous end-joining and homologous recombination repair pathways.The Journal of biological chemistry · 2020Article
- WEE1 inhibition enhances sensitivity to hypoxia/reoxygenation in HeLa cells.Journal of radiation research · 2019Article
- How Cells Handle DNA Breaks during Mitosis: Detection, Signaling, Repair, and Fate Choice.Cells · 2019Review
- HP1α targets the chromosomal passenger complex for activation at heterochromatin before mitotic entry.The EMBO journal · 2018Article
- Article
- Mitotic Vulnerability in Triple-Negative Breast Cancer Associated with LIN9 Is Targetable with BET Inhibitors.Cancer research · 2017Article
- Article
- Mitotic Catastrophe in BC3H1 Cells following Yessotoxin Exposure.Frontiers in cell and developmental biology · 2017Article
- MAD2γ, a novel MAD2 isoform, reduces mitotic arrest and is associated with resistance in testicular germ cell tumors.Cell cycle (Georgetown, Tex.) · 2016Article
- Antiproliferative Fate of the Tetraploid Formed after Mitotic Slippage and Its Promotion; A Novel Target for Cancer Therapy Based on Microtubule Poisons.Molecules (Basel, Switzerland) · 2016Review
- Paclitaxel targets FOXM1 to regulate KIF20A in mitotic catastrophe and breast cancer paclitaxel resistance.Oncogene · 2016Article
- Antitumor Activity of KW-2450 against Triple-Negative Breast Cancer by Inhibiting Aurora A and B Kinases.Molecular cancer therapeutics · 2015Article
- LATS1 and LATS2 phosphorylate CDC26 to modulate assembly of the tetratricopeptide repeat subcomplex of APC/C.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitotic catastrophe is an important mechanism for the induction of cell death in cancer cells by antineoplastic agents that damage DNA. This process is facilitated by defects in the G1 and G2 checkpoints of the cell cycle that are apparent in most cancer cells and which allow the cells to enter mitosis with DNA damage. We have now characterized the dynamics of mitotic catastrophe induced by DNA-damaging agents in p53-deficient cancer cells. Cells that entered mitosis with DNA damage transiently arrested at metaphase for more than 10 h without segregation of chromosomes and subsequently died directly from metaphase. In those metaphase arrested precatastrophic cells, anaphase-promoting complex appeared to be inactivated and BubR1 was persistently localized at kinetochores, suggesting that spindle checkpoint is activated after the DNA damage. Furthermore, suppression of spindle checkpoint function by BubR1 or Mad2 RNA interference in the DNA damaged cells led to escape from catastrophic death and to subsequent abnormal mitosis. Dysfunction of the spindle checkpoint in p53-deficient cancer cells is thus likely a critical factor in resistance to DNA-damaging therapeutic agents.
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Registered trials
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.