Video Experimental Relacionado

Updated: Jan 29, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

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Enzimas modificadoras de histonas como impulsores y dianas terapéuticas en el cáncer de próstata resistente a los

Tanaya A Purohit^1,2, Kayla Bahr¹, Bing Yang¹

¹Department of Urology, School of Medicine and Public Health, University of Wisconsin, Madison, WI, United States.

Frontiers in endocrinology

|January 28, 2026

Abstract:

Androgen deprivation therapy (ADT) remains the cornerstone of treatment for advanced, hormone-sensitive prostate cancer (HSPC), but responses are transient, and most patients ultimately develop castration-resistant prostate cancer (CRPC), a largely incurable stage of disease. The mechanisms driving resistance are not yet fully understood. Recent data suggest epigenetic dysregulation driven by alterations in chromatin remodelers and histone-modifying enzymes (HMEs) contributes significantly to prostate cancer (PC) progression and resistance to androgen-directed therapies. HMEs control chromatin structure and transcriptional programs, and their altered activity contributes to androgen resistance and tumor progression. HME inhibitors offer promising therapeutic potential, yet their effects are highly context-dependent, emphasizing the importance of biomarker-guided precision strategies and rational combination therapies. This review highlights the contribution of histone PTMs and HMEs to CRPC progression and discusses their potential as novel strategies to improve clinical outcomes.

Palabras clave:

sobreexpresión de EZH2 NSD2 resistencia a andrógenos cáncer de próstata resistente a la castración epigenética (remodelación de la cromatina)acetilación de histonas metilación de histonas cáncer de próstata

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