ReviewInternational journal of molecular sciences2017
Cytokinesis Failure Leading to Chromosome Instability in v-Src-Induced Oncogenesis.
Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- RAC1 signaling in polyploid giant cancer cells: Implications for tumorigenesis and therapy resistance.Cancer letters · 2026Review
- The dual role of whole-genome duplication: biological mechanisms, functional consequences, and detection advances.Acta biochimica et biophysica Sinica · 2025Review
- Review
- Whole-Genome Doubling as a source of cancer: how, when, where, and why?Frontiers in cell and developmental biology · 2023Review
- Polo-Like Kinase 4's Critical Role in Cancer Development and Strategies for Plk4-Targeted Therapy.Frontiers in oncology · 2021Review
- The CINs of Polo-Like Kinase 1 in Cancer.Cancers · 2020Review
- Anillin facilitates cell proliferation and induces tumor growth of hepatocellular carcinoma via miR-138/SOX4 axis regulation.Translational oncology · 2020Article
- Src Family Tyrosine Kinases in Intestinal Homeostasis, Regeneration and Tumorigenesis.Cancers · 2020Review
- Abnormal mitosis in reactive astrocytes.Acta neuropathologica communications · 2020Article
- Altering microtubule dynamics is synergistically toxic with spindle assembly checkpoint inhibition.Life science alliance · 2020Article
- The tyrosine kinase v-Src causes mitotic slippage by phosphorylating an inhibitory tyrosine residue of Cdk1.The Journal of biological chemistry · 2018Article
- Role of Membrane Cholesterol Levels in Activation of Lyn upon Cell Detachment.International journal of molecular sciences · 2018Review
- v-Src-driven transformation is due to chromosome abnormalities but not Src-mediated growth signaling.Scientific reports · 2018Article
- Intrinsic and chemically-induced daughter number variations in cancer cell lines.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
v-Src, an oncogene found in Rous sarcoma virus, is a constitutively active variant of c-Src. Activation of Src is observed frequently in colorectal and breast cancers, and is critical in tumor progression through multiple processes. However, in some experimental conditions, v-Src causes growth suppression and apoptosis. In this review, we highlight recent progress in our understanding of cytokinesis failure and the attenuation of the tetraploidy checkpoint in v-Src-expressing cells. v-Src induces cell cycle changes-such as the accumulation of the 4N cell population-and increases the number of binucleated cells, which is accompanied by an excess number of centrosomes. Time-lapse analysis of v-Src-expressing cells showed that cytokinesis failure is caused by cleavage furrow regression. Microscopic analysis revealed that v-Src induces delocalization of cytokinesis regulators including Aurora B and Mklp1. Tetraploid cell formation is one of the causes of chromosome instability; however, tetraploid cells can be eliminated at the tetraploidy checkpoint. Interestingly, v-Src weakens the tetraploidy checkpoint by inhibiting the nuclear exclusion of the transcription coactivator YAP, which is downstream of the Hippo pathway and its nuclear exclusion is critical in the tetraploidy checkpoint. We also discuss the relationship between v-Src-induced chromosome instability and growth suppression in v-Src-induced oncogenesis.
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