{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nZFX is a highly conserved zinc finger transcription factor encoded on the X chromosome that plays a central role in normal stem cell biology. In embryonic and hematopoietic stem cells its expression is essential for self‐renewal and maintenance, and similar “stemness” properties have been demonstrated in cancer stem cell populations. In human embryonic stem cells, for instance, ZFX functions as a molecular rheostat that balances self‐renewal and differentiation, whereas genetic deletion studies in cellular models have identified discrete zinc finger domains that mediate its DNA binding and transactivation functions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNumerous studies have revealed that ZFX is aberrantly overexpressed across a wide range of human cancers. For example, in laryngeal squamous cell carcinoma, gastric cancer, non‐small cell lung cancer, gallbladder carcinoma, renal carcinoma, colorectal cancer, and nasopharyngeal carcinoma, elevated ZFX expression is frequently linked with enhanced tumor aggressiveness, advanced clinical stage, metastasis, and poor prognosis. Similar observations have also been made in tongue squamous cell carcinomas, where ZFX overexpression correlates with tumor grade and shorter survival. In some cases, even germline variants in ZFX have been associated with syndromic intellectual disability that features dysmorphic and endocrine anomalies, emphasizing its clinical relevance across both developmental and oncogenic contexts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, ZFX acts as a bona fide transcriptional activator that binds predominantly to CpG island promoters, often at characteristic positions downstream of the transcription start site. In prostate cancer, for example, ZFX cooperates with oncogenic splice variants of the androgen receptor to regulate a non‐canonical gene expression program, while in glioblastoma it directly binds and activates the c‐Myc promoter to sustain the self‐renewal capacity of tumor‐propagating cells. In hepatocellular carcinoma, ZFX has been shown to transcriptionally upregulate pluripotency mediators such as Nanog and SOX‑2, thereby promoting cancer cell stemness and chemoresistance. Moreover, several studies have highlighted that ZFX levels are modulated by non‑coding RNAs: its expression can be suppressed by tumor‐suppressive microRNAs (for example, miR‑144 and miR‑218) and by long non‑coding RNAs (such as SNHG20) that act as competing endogenous RNAs. Other mechanistic insights include its involvement in the activation of the PI3K/AKT pathway in chronic myeloid leukemia and endometrial cancer, as well as its regulation of glycoprotein galactosylation via B4GALT1 in leukemic cells. Collectively, these data emphasize that ZFX functions as a multifaceted regulator of transcription and signaling that drives oncogenic transformation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn summary, ZFX emerges as a pivotal transcriptional regulator that underpins both the self‑renewal of normal stem cells and the survival, proliferation, and chemoresistance of malignant cells. Its frequent overexpression and association with aggressive tumor phenotypes across diverse neoplasms—from solid tumors such as gastric, lung, colorectal, hepatocellular, and head and neck cancers, to hematologic malignancies including leukemia—highlight its potential as a prognostic biomarker and therapeutic target. Moreover, the regulation of ZFX by non‑coding RNAs and its consequential modulation of key oncogenic pathways underscore the complexity of its role in tumor biology and suggest that targeted interventions aimed at disrupting ZFX function may offer a novel strategy in cancer therapy.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Youxin Zhou, Zuopeng Su, Yulun Huang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The Zfx gene is expressed in human gliomas and is important in the proliferation and apoptosis of the human malignant glioma cell line U251."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Exp Clin Cancer Res (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1186/1756-9966-30-114"}], "href": "https://doi.org/10.1186/1756-9966-30-114"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22185393"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22185393"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Sivan Harel, Edmund Y Tu, Stuart Weisberg, et al. "}, {"type": "b", "children": [{"type": "t", "text": "ZFX controls the self-renewal of human embryonic stem cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0042302"}], "href": "https://doi.org/10.1371/journal.pone.0042302"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22879936"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22879936"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Weiya Ni, Andrew A Perez, Shannon Schreiner, et al. 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