ABSTRACT Prostate cancer is one of the most common cancers in men over the age of sixty. Lysine acetyltransferase 5 (KAT5) is a histone acetyltransferase involved in transcriptional regulation, DNA repair, and cell signaling pathways. Previous studies have shown that KAT5 expression is reduced in the cytoplasm of the prostate cancer cell line LNCaP when exposed to androgen. Moreover, KAT5 has been reported to have a role in the molecular pathway leading to androgen-independent prostate cancer after long-term androgen deprivation therapy. Here, we showed that KAT5 expression was significantly reduced in prostate cancer tissues and cell lines by using the public databases Oncomine and Human Protein Atlas. Reduced KAT5 expression was significantly associated with high mortality in prostate cancer patients. Furthermore, KAT5 overexpression increased the level of apoptotic markers, such as cleaved-caspase 3, in LNCaP cells, thus enhancing the apoptotic death of LNCaP cells. Taken together, KAT5 induced apoptosis in prostate cancer cells via the caspase-3 pathway, indicating that KAT5 could be a gene therapy target for prostate cancer.

中文翻译：

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KAT5 通过半胱天冬酶 3 依赖性细胞凋亡通路负调控前列腺癌 LNCaP 细胞的增殖

摘要 前列腺癌是 60 岁以上男性最常见的癌症之一。赖氨酸乙酰转移酶 5 (KAT5) 是一种组蛋白乙酰转移酶，参与转录调控、DNA 修复和细胞信号通路。先前的研究表明，当暴露于雄激素时，KAT5 在前列腺癌细胞系 LNCaP 的细胞质中表达降低。此外，据报道，KAT5 在长期雄激素剥夺治疗后导致雄激素非依赖性前列腺癌的分子途径中起作用。在这里，我们通过使用公共数据库 Oncomine 和人类蛋白质图谱显示 KAT5 表达在前列腺癌组织和细胞系中显着降低。KAT5 表达降低与前列腺癌患者的高死亡率显着相关。此外，KAT5 过表达增加了 LNCaP 细胞中凋亡标志物的水平，例如裂解的半胱天冬酶 3，从而增强了 LNCaP 细胞的凋亡死亡。总之，KAT5 通过 caspase-3 途径诱导前列腺癌细胞凋亡，表明 KAT5 可能是前列腺癌的基因治疗靶点。