LKB1 inactivation unleashes prostate cancer lineage plasticity  

作　　者：Shaghayegh Nouruzi Amina Zoubeidi 

机构地区：[1]Department of Urologic Sciences,University of British Columbia,Vancouver,BC V5Z 1M9,Canada [2]Vancouver Prostate Centre,Vancouver,BC V6H 3Z6,Canada.

出　　处：《Cell Research》2025年第1期5-6,共2页细胞研究(英文版)

摘　　要：While it is well established that androgen receptor pathway inhibition leads to the development of double-negative prostate cancer(DNPC),the mechanisms underlying this cell fate decision remain unclear.In a recent study published in Cell Research,Li et al.identified that LKB1 inactivation supports the development of DNPC through metabolic and epigenetic rewiring,highlighting DNA hypomethylation as a vulnerability and TET2/3 as potential therapeutic targets.Lineage plasticity contributes to treatment resistance by establishing an alternative identity,as seen in castration-resistant prostate cancer(CRPC)treated with androgen receptor(AR)pathway inhibitors(ARPIs).In a subset of patients,an AR-independent phenotype emerges,with a subtype characterized by loss of AR and expression of squamous markers rather than neuronal markers,known as double-negative prostate cancer(DNPC).1 DNPC is clinically and molecularly distinct from other subtypes and is associated with the worst survival outcomes among metastatic CRPC patients treated with ARPIs.

关 键 词：LKB1 CANCER 

分 类 号：R737.25[医药卫生—肿瘤]