{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nS100A14, an EF‐hand calcium‐binding protein, exerts multifaceted and context‐dependent functions in esophageal carcinomas. Extracellularly, at low concentrations it promotes cell proliferation and survival through binding to RAGE and subsequent activation of ERK1/2 MAPK and NF‑κB pathways, whereas at high doses it triggers mitochondrial pathway–mediated apoptosis via caspase activation. In parallel, intracellular S100A14 influences cell motility and invasiveness by modulating matrix metalloproteinase‑2 (MMP‑2) expression in a p53‐dependent manner and can induce G1 cell cycle arrest and differentiation through upregulation of p21 and nuclear accumulation of p53."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn breast cancer, S100A14 modulates tumor progression through direct interaction with HER2, affecting its phosphorylation and downstream PI3K/AKT and MAPK/ERK signaling cascades. Its aberrant expression contributes to enhanced metastatic potential by upregulating chemokines (namely CCL2 and CXCL5) via a RAGE‐NF‑κB axis, and in triple‐negative breast cancer, elevated S100A14 serves as an independent prognostic indicator of poor clinical outcome. Serum levels of S100A14 further show promise as a non‐invasive diagnostic biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn colorectal cancer, diminished S100A14 expression is associated with poor cellular differentiation and a more aggressive, metastatic phenotype—especially when coupled with elevated levels of S100A4—thereby underscoring its value as a prognostic marker."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn gastric cancer, S100A14 promotes cellular differentiation by upregulating adhesion molecules such as E‑cadherin and PGII, while simultaneously inhibiting cell migration and invasion. This inhibition is mediated, at least in part, through attenuation of store‐operated Ca²⁺ influx and subsequent downregulation of matrix metalloproteinases."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn nasopharyngeal carcinoma, S100A14 functions as a metastasis suppressor by promoting the ubiquitin–proteasome degradation of IRAK1. This, in turn, inhibits NF‑κB signaling and reverses the epithelial–mesenchymal transition, correlating with improved overall and metastasis‐free survival."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn ovarian cancer, particularly in epithelial ovarian malignancies, S100A14 overexpression is linked to enhanced tumorigenesis through activation of the PI3K/Akt pathway, resulting in increased cell proliferation, migration, and invasion, as well as association with advanced stage and poor tumor grade. Moreover, S100A14 forms part of a gene signature predictive for recurrence in serous ovarian carcinoma."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nStudies in lung adenocarcinoma have highlighted the prognostic significance of S100A14 expression; however, its precise functional contributions to tumorigenesis in this context remain to be fully elucidated."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn pancreatic ductal adenocarcinoma, S100A14 exhibits prominent oncogenic properties by promoting cell proliferation, colony formation, migration, invasion, and tumor growth, while also conferring chemoresistance. Notably, elevated S100A14 modulates the tumor immune microenvironment—reducing CD8⁺ T cell infiltration and upregulating PD‑L1 expression—and may therefore serve as a predictive biomarker for responsiveness to immunotherapy."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn prostate cancer, S100A14 appears to act as a tumor suppressor by inhibiting cell proliferation, motility, and the epithelial–mesenchymal transition. This suppressive effect is mediated through the upregulation of FAT1 and consequent activation of the Hippo pathway, with further modulation by transcriptional regulators such as TP63—whose activity can be impeded by CTBP1‑AS to reduce S100A14 expression and promote an oncogenic phenotype."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn oral squamous cell carcinoma, S100A14 functions as a differentiation marker with tumor‐suppressive properties. It influences cellular behavior by interacting with S100A16 and modulating post‐transcriptional regulatory pathways alongside p53 and p21, thereby contributing to growth inhibition and improved differentiation and offering potential as a prognostic indicator."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Qing'e Jin, Hongyan Chen, Aiping Luo, et al. 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