ArticleMolecular oncology2021
Irradiation-induced polyploid giant cancer cells are involved in tumor cell repopulation via neosis.
Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 64 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
- The Sleeping Giant: Metabolism and Autophagy in the Generation and Survival of Dormant Polyploid Giant Cancer Cells.MedComm · 2026Review
- Tetraploids or polyploid giants: who is truly dangerous?Trends in cell biology · 2026Review
- Rewiring cancer cell fate toward vasculogenic mimicry: from classical to unconventional processes.Cancer metastasis reviews · 2026Review
- Clinical Implications of Polyploid Giant Cancer Cells in Solid Tumors: Biology, Diagnosis, and Therapeutic Considerations.Cancers · 2026Review
- CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer.Translational lung cancer research · 2026Article
- Cell Mechanics in Cancer: Integrating Mechanotransduction Pathways Within the Tumor Microenvironment.Journal of cellular physiology · 2026Review
- Radiation-induced autophagy regulates fibroblast mitochondrial metabolism and crosstalk with triple-negative breast cancer cells.Cell reports · 2026Article
- Disrupting Lipid Raft Microdomains to Block Polyploid Giant Cancer Cell Budding and Enhance Radiotherapy Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Etiology of polyploid giant cancer cells: a new frontier in cancer biology.Cancer cell international · 2026Review
- Distinct p21 dynamics drive alternative routes to whole-genome duplication through a common CDK4/6-dependent polyploid G0 state.bioRxiv : the preprint server for biology · 2026Article
- Activation of NF-κB signaling pathway in GSDME-low esophageal squamous cell carcinoma cells enhances radioresistance.Journal of translational medicine · 2026Article
- Genomic Reshuffling After Cell Fusion: Catalyst for Cancer Evolution and Progression.Advances in experimental medicine and biology · 2026Review
- Cross-talk between cancer-associated fibroblasts and dormant cancer cells: current status and promising therapeutic potential.Cancer cell international · 2025Review
- Modelling the monstrosities: experimental and computational systems for studying polyploid giant cancer cells.Expert reviews in molecular medicine · 2025Review
- Decoding cancer dormancy: integrative genomic, phenotypic and live-cell imaging analysis to reveal the hidden cancer cell reservoir.Molecular cancer · 2025Review
- The Impact of Polyploid Giant Cancer Cells: The Root of Stress Resilience.Cancer science · 2025Review
- Aurora Kinase A and B inhibition abrogates 'Neosis', a non-mitotic cell division of GBM residual cells and prevents GBM recurrence.Oncogene · 2025Article
- miR-1246 enhances chemo-resistance of polyploid giant cancer cells in H1299 cells by targeting GSK3β/β-catenin.Discover oncology · 2025Article
- Cells in the Polyaneuploid Cancer Cell State Are Prometastatic.Molecular cancer research : MCR · 2025Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor repopulation occurs when residual tumor cells surviving therapies tenaciously proliferate and re-establish the tumor. The cellular and molecular mechanisms underlying this process remain poorly understood. In this study, we propose that polyploid giant cancer cells (PGCCs) are involved in tumor repopulation via neosis following radiotherapy. We found that although the majority of PGCCs induced by irradiation underwent cell death, some PGCCs exhibited proliferative capacity. Utilizing time-lapse microscopy and single-cell cloning assays, we observed that proliferating PGCCs underwent neosis, thereby contributing to tumor cell repopulation after irradiation. Notably, HMGB1 released from dying tumor cells rather than intracellular HMGB1 could promote neosis-based tumor repopulation, and the latter could be suppressed by the use of HMGB1 inhibitors. Taken together, our results indicate that PGCC can initiate tumor repopulation via neosis following radiation therapy.
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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.