ArticleInternational journal of molecular sciences2016
v-Src Causes Chromosome Bridges in a Caffeine-Sensitive Manner by Generating DNA Damage.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Whole-Genome Doubling as a source of cancer: how, when, where, and why?Frontiers in cell and developmental biology · 2023Review
- Rad17 Translocates to Nucleolus upon UV Irradiation through Nucleolar Localization Signal in the Central Basic Domain.International journal of molecular sciences · 2022Article
- The tyrosine kinase v-Src modifies cytotoxicities of anticancer drugs targeting cell division.Journal of cellular and molecular medicine · 2021Article
- The tyrosine kinase v-Src causes mitotic slippage by phosphorylating an inhibitory tyrosine residue of Cdk1.The Journal of biological chemistry · 2018Article
- Cell-intrinsic and -extrinsic mechanisms promote cell-type-specific cytokinetic diversity.eLife · 2018Article
- v-Src-driven transformation is due to chromosome abnormalities but not Src-mediated growth signaling.Scientific reports · 2018Article
- Cytokinesis Failure Leading to Chromosome Instability in v-Src-Induced Oncogenesis.International journal of molecular sciences · 2017Review
- DNA Damage and Repair in Degenerative Diseases 2016.International journal of molecular sciences · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An increase in Src activity is commonly observed in epithelial cancers. Aberrant activation of the kinase activity is associated with malignant progression. However, the mechanisms that underlie the Src-induced malignant progression of cancer are not completely understood. We show here that v-Src, an oncogene that was first identified from a Rous sarcoma virus and a mutant variant of c-Src, leads to an increase in the number of anaphase and telophase cells having chromosome bridges. v-Src increases the number of γH2AX foci, and this increase is inhibited by treatment with PP2, a Src kinase inhibitor. v-Src induces the phosphorylation of KAP1 at Ser824, Chk2 at Thr68, and Chk1 at Ser345, suggesting the activation of the ATM/ATR pathway. Caffeine decreases the number of cells having chromosome bridges at a concentration incapable of inhibiting Chk1 phosphorylation at Ser345. These results suggest that v-Src induces chromosome bridges via generation of DNA damage and the subsequent DNA damage response, possibly by homologous recombination. A chromosome bridge gives rise to the accumulation of DNA damage directly through chromosome breakage and indirectly through cytokinesis failure-induced multinucleation. We propose that v-Src-induced chromosome bridge formation is one of the causes of the v-Src-induced malignant progression of cancer cells.
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