Epigenetic regulation of androgen dependent and independent prostate cancer.

Advances in cancer research Pub Date : 2024-01-01 Epub Date: 2024-06-06 DOI:10.1016/bs.acr.2024.05.007
Jagdish Mishra, Subhajit Chakraborty, Piyasa Nandi, Soumen Manna, Tirthankar Baral, Niharika, Ankan Roy, Prahallad Mishra, Samir Kumar Patra
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Abstract

Prostate cancer is one of the most common malignancies among men worldwide. Besides genetic alterations, epigenetic modulations including DNA methylation, histone modifications and miRNA mediated alteration of gene expression are the key driving forces for the prostate tumor development and cancer progression. Aberrant expression and/or the activity of the epigenetic modifiers/enzymes, results in aberrant expression of genes involved in DNA repair, cell cycle regulation, cell adhesion, apoptosis, autophagy, tumor suppression and hormone response and thereby disease progression. Altered epigenome is associated with prostate cancer recurrence, progression, aggressiveness and transition from androgen-dependent to androgen-independent phenotype. These epigenetic modifications are reversible and various compounds/drugs targeting the epigenetic enzymes have been developed that are effective in cancer treatment. This chapter focuses on the epigenetic alterations in prostate cancer initiation and progression, listing different epigenetic biomarkers for diagnosis and prognosis of the disease and their potential as therapeutic targets. This chapter also summarizes different epigenetic drugs approved for prostate cancer therapy and the drugs available for clinical trials.

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雄激素依赖型和独立型前列腺癌的表观遗传调控。
前列腺癌是全球男性最常见的恶性肿瘤之一。除基因改变外,包括 DNA 甲基化、组蛋白修饰和 miRNA 介导的基因表达改变在内的表观遗传修饰是前列腺肿瘤发生和癌症进展的主要驱动力。表观遗传修饰因子/酶的异常表达和/或活性导致参与 DNA 修复、细胞周期调控、细胞粘附、细胞凋亡、自噬、肿瘤抑制和激素反应的基因异常表达,从而导致疾病进展。表观基因组的改变与前列腺癌的复发、进展、侵袭性以及从依赖雄激素表型向不依赖雄激素表型的转变有关。这些表观遗传修饰是可逆的,目前已开发出多种针对表观遗传酶的化合物/药物,可有效治疗癌症。本章重点介绍前列腺癌发生和发展过程中的表观遗传学改变,列出用于诊断和预后的不同表观遗传学生物标志物及其作为治疗靶点的潜力。本章还总结了已批准用于前列腺癌治疗的不同表观遗传药物以及可用于临床试验的药物。
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Advancements in computer vision and pathology: Unraveling the potential of artificial intelligence for precision diagnosis and beyond. Deciphering the genetic and epigenetic architecture of prostate cancer. Epigenetic regulation of androgen dependent and independent prostate cancer. Molecular landscape of prostate cancer bone metastasis. Multiplexed quantitative proteomics in prostate cancer biomarker development.
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