Drug-resilient Cancer Cell Phenotype Is Acquired via Polyploidization Associated with Early Stress Response Coupled to HIF2α Transcriptional Regulation.
Christopher CarrollAuraya ManaprasertsakArthur Boffelli CastroHilda van den BosDiana Carolina Johanna SpieringsRene WardenaarAnuraag BukkuriNiklas EngströmEtienne BaratchartMinjun YangAndrea BiloglavCharlie Kinahan CornwallisBertil JohanssonCatharina HagerlingMarie Arsenian HenrikssonKajsa PaulssonSarah R AmendSofie MohlinFloris FoijerAlan McIntyreKenneth J PientaEmma U HammarlundPublished in: Cancer research communications (2024)
In response to cisplatin treatment, some surviving cancer cells undergo whole-genome duplications without mitosis, which represents a mechanism of drug resistance. This study presents mechanistic data to implicate AP-1 and HIF2α signaling in the formation of this surviving cell phenotype. The results open a new avenue for targeting drug-resistant cells.
Keyphrases
- drug resistant
- multidrug resistant
- acinetobacter baumannii
- induced apoptosis
- endothelial cells
- single cell
- cell cycle arrest
- minimally invasive
- electronic health record
- transcription factor
- cancer therapy
- oxidative stress
- emergency department
- drug delivery
- stem cells
- deep learning
- adverse drug
- bone marrow
- cell proliferation
- artificial intelligence
- data analysis