Guo Xiaoqiang, Zhang Qiaoxia
State Engineering Laboratory of Medical Key Technologies Application of Synthetic Biology, Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
Department of Urology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China.
J Kidney Cancer VHL. 2017 May 3;4(2):1-5. doi: 10.15586/jkcvhl.2017.56. eCollection 2017.
Renal cell carcinoma (RCC), the most common kidney cancer, is responsible for more than 100,000 deaths per year worldwide. The molecular mechanism of RCC is poorly understood. Many studies have indicated that epigenetic changes such as DNA methylation, noncoding RNAs, and histone modifications are central to the pathogenesis of cancer. Histone demethylases (KDMs) play a central role in histone modifications. There is emerging evidence that KDMs such as KDM3A, KDM5C, KDM6A, and KDM6B play important roles in RCC. The available literature suggests that KDMs could promote RCC development and progression hypoxia-mediated angiogenesis pathways. Small-molecule inhibitors of KDMs are being developed and used in preclinical studies; however, their clinical relevance is yet to be established. In this mini review, we summarize our current knowledge on the putative role of histone demethylases in RCC.
肾细胞癌（RCC）是最常见的肾癌，在全球范围内每年导致超过10万人死亡。RCC的分子机制尚不清楚。许多研究表明，DNA甲基化、非编码RNA和组蛋白修饰等表观遗传变化是癌症发病机制的核心。组蛋白去甲基化酶（KDMs）在组蛋白修饰中起核心作用。越来越多的证据表明，KDM3A、KDM5C、KDM6A和KDM6B等KDMs在RCC中起重要作用。现有文献表明，KDMs可通过缺氧介导的血管生成途径促进RCC的发展和进展。KDMs的小分子抑制剂正在研发并用于临床前研究；然而，它们的临床相关性尚未确立。在本综述中，我们总结了目前关于组蛋白去甲基化酶在RCC中假定作用的知识。
