{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSERPINB5 (maspin) is a non‐inhibitory member of the serpin family that functions as a multifaceted tumor suppressor in a wide array of human cancers. In many studies maspin has been shown to restrict tumor progression by reducing cell invasion and motility, in part through its ability to interfere with pericellular plasminogen activation and to interact with extracellular matrix components such as collagen. Moreover, maspin is transcriptionally regulated by p53 and other factors, and its expression modulates apoptotic sensitivity, oxidative stress (via its interaction with glutathione S‐transferase) and even the epithelial–mesenchymal transition through partners like IRF6. Its subcellular distribution—with nuclear maspin being associated with improved prognoses—is critical for its role in directly regulating metastasis‐linked gene expression. These studies underscore maspin’s anti‐invasive, pro‐apoptotic and anti‐angiogenic roles in various tumor types such as ovarian, breast, prostate and non‐small cell lung cancers, and highlight its function as both a diagnostic and prognostic marker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to these functional activities, the expression of SERPINB5 is tightly controlled by epigenetic mechanisms. Aberrant DNA methylation patterns at the maspin promoter—whether hypomethylation leading to its de‐repression in certain cancers or promoter hypermethylation associated with gene silencing—have been documented in pancreatic, gastric and other carcinomas. Genome‐wide and locus‐specific methylation analyses, complemented by histone modification studies, reveal that such epigenetic alterations are instrumental not only in tumorigenesis but also in the regulation of normal developmental processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "33", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in malignant tissues, SERPINB5 is also implicated in non‐cancer settings. In the placenta, for example, maspin displays a dynamic pattern of expression and methylation that correlates with trophoblast invasiveness and is exploited for noninvasive prenatal testing by distinguishing fetal DNA in maternal plasma. Furthermore, maspin has been identified as an autoantigen in T cell–mediated conditions such as psoriasis and may also contribute to metastasis formation in colorectal cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "41", "end_ref": "44"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nStructural studies have provided further insight into maspin’s unique mode of action. Crystallographic analyses have revealed that maspin adopts the classical serpin fold with a distinctive reactive center loop that appears to dictate its binding interactions. In parallel, therapeutic studies demonstrate that treatment with agents such as doxazosin, proteasome inhibitors and cisplatin can upregulate maspin expression, thereby enhancing chemosensitivity in prostate and bladder cancers. These observations point to the potential of pharmacologically modulating SERPINB5 activity and its subcellular localization as part of novel anticancer strategies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "45", "end_ref": "47"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Anil K Sood, Mavis S Fletcher, Lynn M Gruman, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The paradoxical expression of maspin in ovarian carcinoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Clin Cancer Res (2002)"}]}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12231537"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12231537"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Ning Jiang, Yonghong Meng, Suliang Zhang, et al. 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