ArticleCancer research2021
Loss of Aurora Kinase Signaling Allows Lung Cancer Cells to Adopt Endoreplication and Form Polyploid Giant Cancer Cells That Resist Antimitotic Drugs.
Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Loss of JAK1 Function Causes G2-M Cell-Cycle Defects Vulnerable to KIF18A Inhibition.Cancer research · 2026Article
- Etiology of polyploid giant cancer cells: a new frontier in cancer biology.Cancer cell international · 2026Review
- Modelling the monstrosities: experimental and computational systems for studying polyploid giant cancer cells.Expert reviews in molecular medicine · 2025Review
- Targeting asymmetric division in cancer stem cells: implications for relapse and resistance.Cancer cell international · 2025Review
- Aurora Kinase A inhibitor alisertib failed to exert its efficacy on TNBC cells due to consequential enrichment of polyploid giant cancer cells (PGCCs).Discover oncology · 2025Article
- ITGB6 promotes tumor recurrence and metastasis by mediating the resistance of daughter cells of PGCCs to anoikis : ITGB6 promotes tumor recurrence and metastasis via Anoikis resistance.Scientific reports · 2025Article
- Cells in the Polyaneuploid Cancer Cell State Are Prometastatic.Molecular cancer research : MCR · 2025Article
- Meeting report: 1st international conference on polyploid giant cancer cells-biology, clinical applications, and the birth of a new field in cancer research.Cancer letters · 2025Article
- Cells in the Polyaneuploid Cancer Cell State are Pro-Metastatic.bioRxiv : the preprint server for biology · 2024Article
- Discovery of a Novel Pseudo-Natural Product Aurora Kinase Inhibitor Chemotype through Morphological Profiling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Inhibition of Aurora B kinase (AURKB) enhances the effectiveness of 5-fluorouracil chemotherapy against colorectal cancer cells.British journal of cancer · 2024Article
- Functional consequences of somatic polyploidy in development.Development (Cambridge, England) · 2024Review
- Dormant cancer cells and polyploid giant cancer cells: The roots of cancer recurrence and metastasis.Clinical and translational medicine · 2024Review
- Polyploid Cancer Cell Models in Drosophila.Genes · 2024Review
- The Importance of Monitoring Non-clonal Chromosome Aberrations (NCCAs) in Cancer Research.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Polyploid giant cancer cells: origin, possible pathways of formation, characteristics, and mechanisms of regulation.Frontiers in cell and developmental biology · 2024Review
- Single-cell morphological and transcriptome analysis unveil inhibitors of polyploid giant breast cancer cells in vitro.Communications biology · 2023Article
- Molecular mechanism of vimentin nuclear localization associated with the migration and invasion of daughter cells derived from polyploid giant cancer cells.Journal of translational medicine · 2023Article
- Targeting BCL2 Overcomes Resistance and Augments Response to Aurora Kinase B Inhibition by AZD2811 in Small Cell Lung Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Cells in the polyaneuploid cancer cell (PACC) state have increased metastatic potential.Clinical & experimental metastasis · 2023Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Polyploid giant cancer cells (PGCC) are common in tumors and have been associated with resistance to cancer therapy, tumor relapse, malignancy, immunosuppression, metastasis, cancer stem cell production, and modulation of the tumor microenvironment. However, the molecular mechanisms that cause these cells to form are not yet known. In this study, we discover that Aurora kinases are synergistic determinants of a switch from the proliferative cell cycle to polyploid growth and multinucleation in lung cancer cell lines. When Aurora kinases were inhibited together, lung cancer cells uniformly grew into multinucleated PGCCs. These cells adopted an endoreplication in which the genome replicates, mitosis is omitted, and cells grow in size. Consequently, such cells continued to safely grow in the presence of antimitotic agents. These PGCC re-entered the proliferative cell cycle and grew in cell number when treatment was terminated. Thus, PGCC formation might represent a fundamental cellular response to Aurora kinase inhibitors and contributes to therapy resistance or tumor relapse. SIGNIFICANCE: These findings provide a novel insight about how cancer cells respond to Aurora kinase inhibitors and identify a new mechanism responsible for resistance to these agents and other antimitotic drugs.
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