Zhang Jiale, Liu Chenxin, Luo Wenting, Sun Baoqing
Department of Clinical Laboratory, National Center for Respiratory Medicine, National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Guangzhou Laboratory, Guangzhou, China.
Cancer Med. 2025 Apr;14(7):e70786. doi: 10.1002/cam4.70786.
Prostate cancer (PCa) is the second most common cancer in men worldwide, and understanding its molecular mechanisms is crucial for developing effective treatment strategies. SIRT7, a NAD+-dependent histone deacetylase, has emerged as a key regulator in PCa progression due to its roles in chromatin remodeling, DNA repair, and transcriptional regulation. Analysis of 492 PCa samples from The Cancer Genome Atlas (TCGA) via cBioPortal revealed that high SIRT7 expression is associated with poor prognosis in PCa patients. Mechanistically, SIRT7 deacetylates histone H3 at lysine 18 (H3K18Ac), a marker associated with aggressive tumors, suppressing tumor suppressor genes and promoting cancer cell proliferation and survival. Epithelial-mesenchymal transition (EMT) is a cellular biological process in which epithelial cells undergo specific molecular and morphological changes to transform into cells with characteristics of mesenchymal cells. SIRT7 also regulates EMT, and inhibiting SIRT7 in PCa cell lines reduces cell migration and invasion, highlighting its potential as a therapeutic target. In summary, the clinical significance of SIRT7 expression in PCa requires further research to elucidate its mechanisms. Developing specific inhibitors targeting SIRT7's deacetylase activity is a promising therapeutic strategy. SIRT7 plays a crucial role in regulating biological processes such as cell proliferation, cell cycle, and apoptosis in PCa through its epigenetic control of gene expression and maintenance of genomic stability. Therefore, SIRT7 may be a potential therapeutic target for PCa, and its expression could have prognostic value for PCa patients, providing important guidance for clinical monitoring and diagnosis by physicians.
前列腺癌（PCa）是全球男性中第二常见的癌症，了解其分子机制对于制定有效的治疗策略至关重要。SIRT7是一种依赖烟酰胺腺嘌呤二核苷酸（NAD+）的组蛋白脱乙酰酶，由于其在染色质重塑、DNA修复和转录调控中的作用，已成为前列腺癌进展的关键调节因子。通过cBioPortal对来自癌症基因组图谱（TCGA）的492份前列腺癌样本进行分析发现，SIRT7高表达与前列腺癌患者的不良预后相关。从机制上讲，SIRT7使赖氨酸18处的组蛋白H3（H3K18Ac）去乙酰化，H3K18Ac是一种与侵袭性肿瘤相关的标志物，它抑制肿瘤抑制基因，促进癌细胞增殖和存活。上皮-间质转化（EMT）是一种细胞生物学过程，上皮细胞在该过程中经历特定的分子和形态变化，转化为具有间质细胞特征的细胞。SIRT7也调节EMT，在前列腺癌细胞系中抑制SIRT7可减少细胞迁移和侵袭，突出了其作为治疗靶点的潜力。总之，SIRT7在前列腺癌中表达的临床意义需要进一步研究以阐明其机制。开发针对SIRT7脱乙酰酶活性的特异性抑制剂是一种有前景的治疗策略。SIRT7通过对基因表达的表观遗传控制和基因组稳定性的维持，在调节前列腺癌的细胞增殖、细胞周期和凋亡等生物学过程中发挥关键作用。因此，SIRT7可能是前列腺癌的潜在治疗靶点，其表达可能对前列腺癌患者具有预后价值，为医生的临床监测和诊断提供重要指导。
