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.