{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSOX4 is a highly conserved developmental transcription factor whose unique HMG‐box DNA‐binding domain enables it to orchestrate diverse gene networks that regulate cell fate, proliferation and differentiation. Aberrant overexpression of SOX4 has been documented in a wide spectrum of cancers—including prostate, medulloblastoma, acute myeloid leukemia and liver‐initiating cells—where it contributes to tumor initiation and maintenance by reprogramming cellular transcriptional circuitry and, in some contexts, by modulating tumor suppressor pathways such as p53. This master regulator is therefore co‐opted from its normal developmental functions to drive oncogenic transformation and stem cell–like self‐renewal in tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in tumor initiation, SOX4 is a potent inducer of epithelial–mesenchymal transition (EMT) and metastatic progression. Acting downstream of extracellular signals such as transforming growth factor–β (TGF‐β) and inflammatory cues in the tumor microenvironment, SOX4 regulates the expression of genes and cascades (for example, effectors like TMEM2) that promote increased cell migration, invasion and immune evasion. Such actions have been implicated in aggressive phenotypes in lung, breast (including triple‐negative breast cancer), cervical and other cancers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nA number of epigenetic and noncoding RNA mechanisms have emerged as key determinants of SOX4 expression in cancer. In several tumor models—including bladder, endometrial, gastric, and colorectal carcinomas—the loss or altered expression of specific microRNAs (for example, miR‐129–2, miR‐320) as well as long noncoding RNAs (for example, CASC15 and LINC01133) relieves repression of SOX4, thereby enhancing its oncogenic functions. These regulatory circuits affect not only SOX4 levels but also downstream programs such as microRNA processing, with consequent effects on cell survival and therapeutic responsiveness."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, SOX4 plays a dynamic role in mediating cellular stress responses that influence DNA damage repair, cell cycle regulation and chemoresistance. By stabilizing and enhancing p53 activity in response to genotoxic stress, SOX4 enforces cell cycle checkpoints and, in certain contexts, promotes apoptosis; its deregulation is associated with disease recurrence and therapeutic resistance in cancers such as colorectal, hepatocellular and non–small‐cell lung cancer. Targeting the SOX4 axis—either directly or via its upstream modulators (including TGF‐β, NF–κB and MTA1) and associated noncoding RNAs—therefore offers an attractive strategy to overcome drug resistance and improve patient outcomes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "L P van Houte, V P Chuprina, M van der Wetering, et al. 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