{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nWNT16 functions as a paracrine and autocrine mediator in multiple cancer‐related contexts. In tumor microenvironments, WNT16B is upregulated in response to DNA damage and chemotherapy, where its secretion activates canonical Wnt signaling in neighboring cancer cells, thereby promoting cell survival and treatment resistance. In uterine leiomyomas, estrogen and progesterone stimulate mature cells to secrete WNT16, which in turn induces β‐catenin nuclear translocation in tumor‐initiating stem cells. In acute lymphoblastic leukemia with t(1;19) translocation, the E2A–PBX1 fusion protein drives preferential expression of the WNT16B isoform, and its inhibition triggers apoptosis through downregulation of survivin via the canonical Wnt pathway. Moreover, WNT16 has emerged as an important factor in senescence, where its expression is necessary for full p53‐dependent activation of p21 and proper activation of the PI3K/AKT pathway, and it is found upregulated in chronic lymphocytic leukemia as well, suggesting multiple roles in malignant transformation and cellular aging."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the realm of skeletal biology, WNT16 plays a crucial role in regulating bone mass and structure. Osteoblast‐derived WNT16 inhibits osteoclastogenesis both directly and indirectly through upregulation of osteoprotegerin, thereby enhancing cortical bone thickness and lowering fracture risk. Genome‐wide association studies and functional mouse models have consistently linked coding and regulatory variants in WNT16 to variations in cortical and trabecular bone mineral density, bone strength, and skeletal site–specific effects—including associations with lumbar spine, forearm, skull, and hip bone outcomes. Additionally, non‐synonymous polymorphisms in WNT16 are associated with osteoporotic fractures and even influence osteoarthritis phenotypes, underscoring its role as a key regulator of bone formation and resorption."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "24"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence also indicates that WNT16 exerts functions beyond bone and cancer biology. Comparative genomics studies have established that WNT16 is evolutionarily conserved, with two isoforms present in vertebrates. In the immune system, WNT16 positively influences lymphocyte proliferation and has been associated with maintaining higher CD4+ T‐cell counts in HIV infection. Additionally, rare missense variants in WNT16 have been implicated in systemic lupus erythematosus, while a frameshift mutation in a conserved region of WNT16a may alter susceptibility to type 2 diabetes through deregulated canonical signaling. At the maternal–fetal interface, decidual stromal cell–derived WNT16 promotes trophoblast survival and invasion via the AKT/β‐catenin pathway, and reduced levels of circulating WNT16 have been linked to low bone mass in adolescent idiopathic scoliosis. These diverse functions underscore the broad physiological relevance of WNT16 in development, immunity, metabolism, and reproductive biology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "29"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Julien Mazieres, Liang You, Biao He, et al. 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