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Serine protease 56 (PRSS56) is a secreted, trypsin-like serine protease encoded by the PRSS56 gene, characterized by the presence of a peptidase S1 domain and extracellular proteolytic activity[1][2][3]. PRSS56 is a critical regulator of ocular development, particularly by influencing eye axial length and the structure of anterior segment tissues. Mutations in PRSS56 cause autosomal recessive posterior microphthalmos and related syndromes, leading to reduced eye size and increased risk of glaucoma[1][2]. In cancer biology, PRSS56 has been identified as a cancer-testis antigen: it is normally testis-specific but becomes frequently overexpressed in gastric and colorectal cancers due to promoter DNA hypomethylation[3]. Functionally, overexpression of PRSS56 activates the PI3K/AKT pathway in cancer cells, promoting proliferation, migration, and invasion, and may serve as both a therapeutic target and a biomarker for patient selection in certain cancers[3]. No approved drugs currently target PRSS56 directly, but PI3K inhibitors can mitigate its oncogenic effects in cell-based models[3].
Inhibitors block PRSS56-induced PI3K/AKT activation, reducing cancer cell proliferation, migration, and invasion
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