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
- minimally invasive
- single cell
- electronic health record
- transcription factor
- cell therapy
- cancer therapy
- big data
- endoplasmic reticulum stress
- replacement therapy
- machine learning
- signaling pathway
- pseudomonas aeruginosa
- cell proliferation
- drug delivery
- cystic fibrosis
- pi k akt
- bone marrow
- smoking cessation
- adverse drug
- drug induced