ArticleCell cycle (Georgetown, Tex.)2014
JNK signaling is needed to tolerate chromosomal instability.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 24 citations in OpenAlex.
- Chromosomal instability as an architect of the cancer stemness landscape.Frontiers in cell and developmental biology · 2024Review
- Breast cancer stem cells tolerate chromosomal instability during tumor progression via c-Jun/AXL stress signaling.Heliyon · 2023Article
- Mitochondrial RNA methyltransferase TRMT61B is a new, potential biomarker and therapeutic target for highly aneuploid cancers.Cell death and differentiation · 2023Article
- Review
- Co-Operation between Aneuploidy and Metabolic Changes in Driving Tumorigenesis.International journal of molecular sciences · 2019Review
- ZPR1-Dependent Neurodegeneration Is Mediated by the JNK Signaling Pathway.Journal of experimental neuroscience · 2019Article
- Mechanisms regulating immune surveillance of cellular stress in cancer.Cellular and molecular life sciences : CMLS · 2018Review
- Evidence for a novel function of Awd in maintenance of genomic stability.Scientific reports · 2017Article
- Phosphoenolpyruvate Carboxykinase Maintains Glycolysis-driven Growth in Drosophila Tumors.Scientific reports · 2017Article
- Article
- Chromosomal instability triggers cell death via local signalling through the innate immune receptor Toll.Oncotarget · 2015Article
- Article
- Sterile inflammation in Drosophila.Mediators of inflammation · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosomal instability (CIN), as a common feature of tumors, represents a potential therapeutic target if ways can be found to specifically cause apoptosis in unstably dividing cells. We have previously shown that if signaling through the JNK pathway is reduced, apoptosis is triggered in models of chromosomal instability induced by loss of the spindle checkpoint. Here we identify components upstream and downstream of JNK that are able to mediate this effect, and test the involvement of p53 and DNA damage in causing apoptosis when JNK signaling is reduced in CIN cells. We show that cell cycle progression timing has a strong effect on the apoptosis seen when JNK signaling is reduced in genetically unstable cells: a shortened G 2 phase enhances the apoptosis, while lengthening G 2 rescues the JNK-deficient CIN cell death phenotype. Our findings suggest that chromosomal instability represents a significant stress to dividing cells, and that without JNK signaling, cells undergo apoptosis because they lack a timely and effective response to DNA damage.
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What OpenQuestion holds
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.