Super-enhancers mediates SLC7A11 via FOXA1 to regulate disulfidptosis in prostate cancer.

ABSTRACT: Prostate cancer (PCa) remains a major therapeutic challenge due to aberrant androgen receptor signaling and a remodeled tumor microenvironment. Disulfidptosis, a recently identified form of cell death characterized by cytoskeletal collapse under conditions of glucose deprivation and elevated SLC7A11 expression, presents a potential novel avenue for intervention. In this study, we integrated TCGA and GEO data and employed machine learning techniques to identify disulfidptosis-related genes in prostate cancer. Functional analyses using SLC7A11-overexpressing and knockout cell lines demonstrated that SLC7A11 promotes cellular proliferation, migration, and invasion, while its overexpression under glucose-starved conditions triggers disulfidptosis, also inducible pharmacologically using the glu

SUBMITTER: Kang Z 

PROVIDER: S-EPMC12827458 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature