{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSALL4 is a highly conserved zinc‐finger transcription factor that plays an essential role during early embryogenesis by maintaining embryonic stem cell self‐renewal and pluripotency. Mutations in SALL4 underlie congenital malformation syndromes—such as Okihiro syndrome and Duane–radial ray syndrome—demonstrating its pivotal role in normal development. Moreover, experimental reprogramming of somatic cells into pluripotent cells has revealed that SALL4 not only sustains the undifferentiated state but also actively enhances reprogramming efficiency, underscoring its central function in early cell fate determination."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn diverse malignancies, aberrant reactivation of SALL4 endows tumor cells with stem cell–like properties that promote oncogenesis, metastasis, and resistance to therapy. Elevated levels of SALL4 have been detected in hematologic cancers as well as in solid tumors—including testicular germ cell neoplasms, extragonadal yolk sac tumors, gastric carcinoma, breast cancer, hepatocellular carcinoma, colorectal cancer, and gliomas—where its expression correlates with poor clinical outcome. Functionally, SALL4 drives oncogenic signaling (for example via the Wnt/β-catenin pathway), modulates epigenetic regulators, and contributes to cell cycle progression and survival, thereby serving as both a sensitive diagnostic marker and a functional contributor to tumor aggressiveness."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nSALL4 expression and function are further tuned by upstream regulatory mechanisms—including direct transcriptional activation by STAT3 and post‐transcriptional repression by multiple microRNAs (for example, miR‑107, miR‑33b, miR‑219‑5p, and miR‑98)—which link its dysregulation to tumor progression in cancers such as glioma, breast, and colon carcinoma. In addition, SALL4 is subject to pharmacologic targeting through thalidomide‐dependent cereblon-mediated degradation; structural insights into these interactions are now informing the design of safer therapeutic strategies aimed at mitigating SALL4-driven tumorigenesis. Together with its interplay with epigenetic modifiers and its contribution to key signaling cascades (such as Wnt/β‑catenin in cervical cancer), these findings underscore the emerging therapeutic potential of targeting SALL4 in various human malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "46"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jürgen Kohlhase, Marielle Heinrich, Lucia Schubert, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Stem cell factor SALL4 represses the transcriptions of PTEN and SALL1 through an epigenetic repressor complex."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2009)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0005577"}], "href": "https://doi.org/10.1371/journal.pone.0005577"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "19440552"}], "href": "https://pubmed.ncbi.nlm.nih.gov/19440552"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Sha Sha Zeng, Taro Yamashita, Mitsumasa Kondo, et al. 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