{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSUZ12 is a core subunit of the Polycomb Repressive Complex 2 (PRC2) that mediates epigenetic gene silencing by catalyzing trimethylation of histone H3 at lysine 27. This modification is essential for repressing key developmental regulators and maintaining the undifferentiated state of embryonic stem cells. In addition, recent studies further show that SUZ12 can cooperate with other factors and contribute to histone H3K9 methylation in differentiated cells, thereby integrating multiple chromatin‐based regulatory mechanisms."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAlterations in SUZ12 play critical roles in tumorigenesis. Loss-of-function mutations and deletions that inactivate SUZ12 result in a collapse of the H3K27 trimethylation mark in several cancers, including malignant peripheral nerve sheath tumors, T-cell acute lymphoblastic leukemia, and other aggressive neoplasms. In specific contexts such as peripheral nerve sheath tumors and high-grade gliomas, SUZ12 acts as a tumor suppressor, and its loss cooperates with mutations in NF1 and other oncogenic drivers to amplify aberrant Ras signaling. In T-ALL models, diminished PRC2 activity via SUZ12 inactivation contributes to oncogenic transcriptional reprogramming."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAnother recurrent mechanism affecting SUZ12 function is its involvement in chromosomal rearrangements and gene fusions. In endometrial stromal neoplasms, trans-splicing or chromosomal translocations fuse the 5′ exons of JAZF1 with sequences of the Polycomb group gene (historically called JJAZ1 and now recognized as SUZ12), generating chimeric transcripts that have anti-apoptotic activity. The frequency and structure of these JAZF1–SUZ12 fusions differ among classic endometrial stromal tumors compared to various morphologic variants, providing both diagnostic utility and insights into the biology of these tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nPost‐transcriptional regulation of SUZ12 by microRNAs and other epigenetic modifiers also appears to be an important determinant of cancer progression. In breast cancer and lung tumors, downregulation of specific miRNAs such as miR‑200 and miR‑489 results in the upregulation of SUZ12, which then contributes to enhanced H3K27 trimethylation, repression of epithelial markers (for example, E-cadherin), and promotion of cancer stem cell properties, epithelial–mesenchymal transition, and chemoresistance. In epithelial ovarian, gastric, and colorectal cancers, aberrantly high expression of SUZ12 correlates with proliferative capacity, metastatic potential, and poorer clinical outcomes, suggesting its oncogenic role in these settings. Furthermore, in hepatitis B virus–associated hepatocarcinogenesis, oncogenic kinases induce SUZ12 degradation, thereby reprogramming the chromatin landscape."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its oncogenic and tumor‐suppressive roles, alterations in SUZ12 are implicated in developmental disorders. Rare germline mutations in SUZ12 have been associated with Weaver-like overgrowth syndromes characterized by postnatal overgrowth, dysmorphic features, and variable neurodevelopmental deficits. Structural studies of SUZ12 within PRC2 complexes further reveal how its distinct domains mediate interactions with accessory factors, thereby dictating complex composition (PRC2.1 versus PRC2.2) and chromatin occupancy. In addition, signaling pathways such as those mediated by WNT proteins interface with SUZ12 regulation, underscoring its integration in both developmental and cancer-related transcriptional networks."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Tong Ihn Lee, Richard G Jenner, Laurie A Boyer, et al. 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