Abstract
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 via 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.
Highlights
Renal cell carcinoma (RCC) accounts for 2%–3% of all adult malignancies and causes more than 100,000 deaths per year worldwide [1]
KDM5C inactivation can lead to genomic instability in RCC [45]. These findings indicate that several histone demethylases can be induced under hypoxia which in turn regulate the expression of cancer-related genes, and trigger RCC development
Better understanding of the molecular mechanisms that govern RCC development and progression will enable the development of novel compounds
Summary
Renal cell carcinoma (RCC) accounts for 2%–3% of all adult malignancies and causes more than 100,000 deaths per year worldwide [1]. How to cite: Guo X et al The Emerging Role of Histone Demethylases in Renal Cell Carcinoma. KDM3A has been implicated in the development and progression of several malignancies, including hepatocellular carcinoma and gastric cancer [16, 17]. We and other researchers have reported that overexpression of KDM3A is associated with RCC development [18, 19].
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