Yuyin Jiang

γ-H2AX phosphorylated histone H2AX on serine 139 ΔΨm mitochondrial membrane potential AKT protein kinase B ATP adenosine triphosphate CCL2 C-C motif chemokine ligand 2 ChIP chromatin immunoprecipitation CUT and Tag Cleavage Under Targets and Tagmentation EDU 5-Ethynyl-2′-deoxyuridine GO enrichment gene ontology enrichment analysis GSIS glucose-stimulated insulin secretion H2O2 hydrogen peroxide hAMSC human amniotic mesenchymal stem cell HFD high-fat diet IL-1β interleukin-1 beta IL-6...

Abstract Resistance to androgen receptor (AR)-targeted therapies, such as enzalutamide, in castration-resistant prostate cancer (CRPC) remains a significant clinical challenge, often driven by mechanisms including lineage plasticity. The precise molecular mechanisms driving this process, particularly downstream effectors, remain incompletely understood.

Abstract Cancer remains a leading cause of death worldwide, with lineage plasticity emerging as a hallmark that drives therapy resistance and tumor progression, allowing cancer cells to rapidly alter their identity and evade targeted therapies. Although various genomic and transcriptomic aberrations correlate with lineage plasticity, the lack of pan-cancer gene markers quantifying lineage plasticity has limited its utility as a predictive biomarker.