J Cancer 2019; 10(3):721-729. doi:10.7150/jca.28254 This issue
1. Department of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China;
2. National Clinical Research Center for Cancer, Tianjin, China;
3. Key Laboratory of Cancer Prevention and Therapy, Tianjin, China;
4. Tianjin's Clinical Research Center for Cancer, Tianjin, China;
5. Key Laboratory of Cancer Immunology and Biotherapy, Tianjin, China.
Epigenetic modifications at the histone level have attracted significant attention because of their roles in tumorigenesis. Suppressor of variegation 3-9 homolog 2 (SUV39H2, also known as KMT1B) is a member of the SUV39 subfamily of lysine methyltransferases (KMTs) that plays a significant role in histone H3-K9 di-/tri-methylation, transcriptional regulation and cell cycle. Overexpressions of SUV39H2 at gene, mRNA and protein levels are known to be associated with a range of cancers: leukemia, lymphomas, lung cancer, breast cancer, colorectal cancer, gastric cancer, hepatocellular cancer and so on. Accumulating evidence indicates that SUV39H2 acts as an oncogene and contributes to the initiation and progression of cancers. It could, therefore, be a promising target for anti-cancer treatment. In this review, we focus on the dysregulation of SUV39H2 in cancers, including its clinical prognostic predictor role, molecular mechanism involved in cancer occurrence and development, relevant inhibitors against cancer, and its epigenetic modification interaction with immunotherapy. A better understanding of the SUV39H2 will be beneficial to the development of molecular-targeted therapies in cancer.
Keywords: SUV39H2, Histone methyltransferase, epigenetic modification, cancer