Chen Rui, Chen Yan, Zhao Weiqing, Fang Cheng, Zhou Wenjie, Yang Xin, Ji Mei
Department of Oncology, The Third Affiliated Hospital of Soochow University, The First People's Hospital of Changzhou, Changzhou 213003, People's Republic of China.
Onco Targets Ther. 2020 Jul 13;13:6837-6846. doi: 10.2147/OTT.S259873. eCollection 2020.
Malignant solid tumors are the leading cause of death in humans, and epigenetic regulation plays a significant role in studying the mechanism of human solid tumors. Recently, histone lysine methylation has been demonstrated to be involved in the development of human solid tumors due to its epigenetic stability and some other advantages. The 90-kb protein methyltransferase nuclear receptor SET domain-containing 2 (NSD2) is a member of nuclear receptor SET domain-containing (NSD) protein lysine methyltransferase (KMT) family, which can cause epigenomic aberrations via altering the methylation states. Studies have shown that NSD2 is frequently over-expressed in multiple types of aggressive solid tumors, including breast cancer, renal cancer, prostate cancer, cervical cancer, and osteosarcoma, and such up-regulation has been linked to poor prognosis and recurrence. Further studies have identified that over-expression of NSD2 promotes cell proliferation, migration, invasion, and epithelial-mesenchymal transformation (EMT), suggesting its potential oncogenic role in solid tumors. Moreover, Gene Expression Profiling Interactive Analysis (GEPIA) was searched for validation of prognostic value of NSD2 in human solid tumors. However, the underlying specific mechanism remains unclear. In our present work, we summarized the latest advances in NSD2 expression and clinical applications in solid tumors, and our findings provided valuable insights into the targeted therapeutic regimens of solid tumors.
恶性实体瘤是人类死亡的主要原因，表观遗传调控在研究人类实体瘤的机制中起着重要作用。最近，组蛋白赖氨酸甲基化因其表观遗传稳定性和其他一些优势，已被证明参与人类实体瘤的发展。90千碱基的蛋白质甲基转移酶含核受体SET结构域2（NSD2）是含核受体SET结构域（NSD）的蛋白质赖氨酸甲基转移酶（KMT）家族的成员，它可通过改变甲基化状态导致表观基因组畸变。研究表明，NSD2在多种侵袭性实体瘤中频繁过表达，包括乳腺癌、肾癌、前列腺癌、宫颈癌和骨肉瘤，这种上调与预后不良和复发有关。进一步研究发现，NSD2的过表达促进细胞增殖、迁移、侵袭和上皮-间质转化（EMT），提示其在实体瘤中具有潜在的致癌作用。此外，通过搜索基因表达谱交互分析（GEPIA）来验证NSD2在人类实体瘤中的预后价值。然而，其潜在的具体机制仍不清楚。在我们目前的工作中，我们总结了NSD2在实体瘤中的表达及临床应用的最新进展，我们的研究结果为实体瘤的靶向治疗方案提供了有价值的见解。
