{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nWNT7B is a versatile secreted ligand of the Wnt family that plays a critical role in cancer progression. In malignant gliomas, upregulation of WNT7B by Olig2‐positive tumor cells facilitates single‐cell vessel co‐option and blood–brain barrier preservation, thereby contributing to therapeutic resistance. In castration‐resistant prostate cancer, WNT7B is a direct androgen receptor target gene whose high expression is essential for androgen‐independent cell growth and for stimulating osteoblast differentiation that underlies the characteristic osteoblastic bone metastasis. In breast carcinoma, WNT7B produced by tumor‐associated myeloid cells drives an angiogenic switch that promotes tumor progression and metastasis. In pancreatic ductal adenocarcinoma and osteosarcoma, increased WNT7B expression fosters cell autonomous Wnt/β‐catenin activation, leading to enhanced proliferation and survival; additionally, in glioblastoma, both EZH2-dependent mechanisms and a noncoding RNA‐mediated (miR-326) pathway converge on WNT7B to sustain stem cell properties and mediate temozolomide resistance, while interactions between the Frizzled receptor Fzd7 and WNT7B further promote cancer stemness and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its oncogenic functions, WNT7B is indispensably involved in developmental processes, tissue homeostasis, and repair. Mesenchymal stem cells secrete WNT7B to stimulate lung fibroblast proliferation and matrix production—a process that is pivotal in normal lung development as well as in the pathogenesis of pulmonary fibrosis. Aberrant and epigenetically deregulated WNT7B expression has been linked to neural tube defects and is observed in congenital pulmonary airway malformation, indicating a role in early morphogenesis. In the skeletal system, WNT7B enhances self‐renewal and osteogenic differentiation of bone marrow mesenchymal stem cells via a Ca²⁺‐dependent signaling cascade, thereby promoting bone formation. Likewise, in pancreatic progenitor cells, non‐canonical WNT7B/PKC signaling supports cellular proliferation during organ development. Genetic association studies further implicate WNT7B in ocular development, with variants correlating significantly with axial length, corneal curvature, and central corneal thickness, while altered WNT7B expression in psoriatic skin suggests a role in cutaneous homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging studies further extend the functional repertoire of WNT7B into other pathological contexts. In Dupuytren’s contracture, specific polymorphisms in WNT7B are associated with an increased disease risk. In cholangiocarcinoma, photodynamic therapy elicits a p53/miR‑34a‑5p axis that targets WNT7B, thereby modulating tumor cell viability and apoptotic responses. In colorectal cancer, WNT7B promotes cellular proliferation, migration, and invasion. Notably, founder variants in WNT7B have been identified in patients with PDAC syndrome—a congenital condition characterized by pulmonary hypoplasia, diaphragmatic anomalies, anophthalmia/microphthalmia, and cardiac defects—underscoring its critical role in morphogenesis. Finally, regulation of WNT7B by long noncoding RNAs influences muscle stem cell fate decisions, further broadening the spectrum of WNT7B’s biological impact."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Dali Zheng, Keith F Decker, Tianhua Zhou, et al. 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