ArticleClinical & experimental metastasis2019
The role of heterogeneous environment and docetaxel gradient in the emergence of polyploid, mesenchymal and resistant prostate cancer cells.
Article in Clinical & experimental metastasis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 68 citations in OpenAlex.
- RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Balance Between Order and Disorder: Quantum-Epigenetic Pathways for the Emergence and Continuous Evolution of Life.Acta biotheoretica · 2026Review
- Tumor cells escape from therapy-induced senescence: from molecular mechanisms to targeted intervention.Biology direct · 2026Review
- Clinical Implications of Polyploid Giant Cancer Cells in Solid Tumors: Biology, Diagnosis, and Therapeutic Considerations.Cancers · 2026Review
- Prostate Cancer-Associated Fibroblasts: A Review on CAF Functions, Heterogeneity, Resistance Mechanisms, and Future in a Chip.International journal of molecular sciences · 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
- Life history enlightened therapies: cell cycle mapping to identify molecular targets to prevent hepatocellular carcinoma.Evolution, medicine, and public health · 2026Article
- Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.Cancer letters · 2025Article
- Phosphorescence-basediScience · 2025Article
- Oncogenic signaling in the Drosophila prostate-like accessory gland activates a pro-tumorigenic program in the absence of proliferation.Disease models & mechanisms · 2025Article
- Microfluidics-Based Technologies for the Assessment of Castration-Resistant Prostate Cancer.Cells · 2024Review
- Dormant cancer cells and polyploid giant cancer cells: The roots of cancer recurrence and metastasis.Clinical and translational medicine · 2024Review
- The Importance of Monitoring Non-clonal Chromosome Aberrations (NCCAs) in Cancer Research.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Article
- Cell Fusion and Syncytia Formation in Cancer.Results and problems in cell differentiation · 2024Review
- A mathematical investigation of polyaneuploid cancer cell memory and cross-resistance in state-structured cancer populations.Scientific reports · 2023Article
- Cells in the polyaneuploid cancer cell (PACC) state have increased metastatic potential.Clinical & experimental metastasis · 2023Article
- Nuclear morphology predicts cell survival to cisplatin chemotherapy.Neoplasia (New York, N.Y.) · 2023Article
- Targeting polyploid giant cancer cells potentiates a therapeutic response and overcomes resistance to PARP inhibitors in ovarian cancer.Science advances · 2023Article
- Computational Biology Helps Understand How Polyploid Giant Cancer Cells Drive Tumor Success.Genes · 2023Review
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
The ability of a population of PC3 prostate epithelial cancer cells to become resistant to docetaxel therapy and progress to a mesenchymal state remains a fundamental problem. The progression towards resistance is difficult to directly study in heterogeneous ecological environments such as tumors. In this work, we use a micro-fabricated "evolution accelerator" environment to create a complex heterogeneous yet controllable in-vitro environment with a spatially-varying drug concentration. With such a structure we observe the rapid emergence of a surprisingly large number of polyploid giant cancer cells (PGCCs) in regions of very high drug concentration, which does not occur in conventional cell culture of uniform concentration. This emergence of PGCCs in a high drug environment is due to migration of diploid epithelial cells from regions of low drug concentration, where they proliferate, to regions of high drug concentration, where they rapidly convert to PGCCs. Such a mechanism can only occur in spatially-varying rather than homogeneous environments. Further, PGCCs exhibit increased expression of the mesenchymal marker ZEB1 in the same high-drug regions where they are formed, suggesting the possible induction of an epithelial to mesenchymal transition (EMT) in these cells. This is consistent with prior work suggesting the PGCC cells are mediators of resistance in response to chemotherapeutic stress. Taken together, this work shows the key role of spatial heterogeneity and the migration of proliferative diploid cells to form PGCCs as a survival strategy for the cancer population, with implications for new therapies.
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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.