{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSPOCK1 is a secreted, calcium‐binding matricellular proteoglycan that is aberrantly overexpressed in a wide spectrum of human cancers—including hepatocellular carcinoma, gastric, gallbladder, lung, esophageal, prostate, glioma, colorectal, ovarian, pancreatic, and renal carcinomas—and its elevated expression is strongly associated with aggressive tumor behavior. In these malignancies, SPOCK1 promotes key oncogenic processes such as cell proliferation, migration, invasion, epithelial–mesenchymal transition (EMT), and metastasis, and its up‐regulation correlates with poor clinical outcomes and resistance to targeted or conventional therapies. Mechanistic investigations have shown that SPOCK1 functions downstream of transforming growth factor–β (TGF‐β) and other oncogenic signals, activating pathways including PI3K/AKT, Wnt/β‐catenin, mTOR, and NF–κB. In addition, SPOCK1 modulates extracellular matrix remodeling through regulation of matrix metalloproteinases (e.g. MMP‐2) and interacts with transcriptional regulators (such as SIX1 and Slug) to reinforce EMT and aggressive behavior in cancer cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its clear oncogenic roles, SPOCK1 expression is subject to complex regulatory mechanisms that further refine its impact on tumor behavior. Multiple studies have shown that aberrant expression of SPOCK1 can result from—and be modulated by—noncoding RNAs such as microRNAs and long noncoding RNAs, as well as by TGF–β–mediated signaling. Through these mechanisms, SPOCK1 not only drives EMT and extracellular matrix remodeling but also contributes to drug resistance by altering apoptosis and cell cycle control. These multifaceted regulatory networks offer promising avenues for therapeutic intervention by targeting SPOCK1 expression or activity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer, SPOCK1 (also known as Testican‐1) functions in several non‐neoplastic processes. Genetic studies have implicated members of the SPOCK family in developmental events such as the regulation of age at menarche—possibly through modulation of extracellular matrix remodeling and inhibition of key proteases like MMP‐2—as well as in metabolic processes such as adipocyte differentiation. In other settings, increased SPOCK1 levels have been observed in conditions such as drug‐induced gingival overgrowth and systemic inflammatory responses (e.g. sepsis), and structural studies of related family members have provided insight into its modular domain organization that underpins its diverse functions in cellular motility and tissue remodeling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "37", "end_ref": "42"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yan Li, Leilei Chen, Tim Hon Man Chan, et al. 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