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
- cell cycle arrest
- endothelial cells
- single cell
- transcription factor
- minimally invasive
- cancer therapy
- stem cells
- big data
- signaling pathway
- cell death
- mesenchymal stem cells
- oxidative stress
- combination therapy
- pseudomonas aeruginosa
- machine learning
- deep learning
- pi k akt