{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTACSTD2, which encodes Trop‐2, is a multifunctional transmembrane glycoprotein that serves as a calcium signal transducer and is frequently overexpressed in a wide variety of human epithelial cancers. Elevated Trop‐2 expression has been implicated in enhancing cell proliferation, inducing anchorage‐independent growth, and promoting tumorigenesis in malignancies such as colorectal, pancreatic, lung, prostate, and breast cancers. Its deregulation activates intracellular signaling cascades—among them the ERK/MAPK, PI3K/AKT, and JAK2/STAT3 pathways—that drive cell‐cycle progression and confer invasive and metastatic potential, while also contributing to chemoresistance. These oncogenic properties have been reinforced by studies showing that Trop‐2 is required for the maintenance of cancer stem/progenitor cell populations and that its overexpression quantitatively stimulates tumor growth and dissemination."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in promoting cell growth, Trop‐2 critically modulates the tumor microenvironment by affecting cell adhesion and migration. It can interact with key adhesion molecules, including integrins and tight junction proteins, thereby reorganizing cytoskeletal dynamics and facilitating directional migration and metastasis. Differential subcellular localization—membrane‐associated versus intracellular—appears to delineate distinct functional states that correlate with tumor aggressiveness and clinical outcome. Moreover, Trop‐2–driven signaling intersects with pathways regulating cyclin D1 expression and epithelial–mesenchymal transition, further underscoring its impact on the invasive behavior of tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, Trop‐2 plays roles in normal epithelial biology, including the regulation of progenitor cell function and barrier integrity. In certain tissues such as the prostate and corneal epithelium, Trop‐2 aids in subfractionating stem/progenitor populations and maintaining tight junction organization through interactions with claudins. The molecule’s transcriptional regulation is governed by a network of key transcription factors, and its aberrant activation—sometimes exploited therapeutically by antibody–drug conjugates targeting its extracellular domain—underscores its potential as a prognostic biomarker and therapeutic target. Emerging data in diverse cancer types, including cervical, ovarian, glioblastoma, and gastric adenocarcinoma, support the concept that Trop‐2 not only drives malignant progression but also offers a window into personalized therapeutic interventions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "42"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "T El Sewedy, M Fornaro, S Alberti "}, {"type": "b", "children": [{"type": "t", "text": "Cloning of the murine TROP2 gene: conservation of a PIP2-binding sequence in the cytoplasmic domain of TROP-2."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Cancer (1998)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/(sici)1097-0215(19980119)75:2"}, {"type": "a", "children": [{"type": "t", "text": "324::aid-ijc24"}], "href": "324::aid-ijc24"}, {"type": "t", "text": "3.0.co;2-b"}], "href": "https://doi.org/10.1002/(sici"}, {"type": "t", "text": "1097-0215(19980119)75:2"}, {"type": "a", "children": [{"type": "t", "text": "324::aid-ijc24"}], "href": "324::aid-ijc24"}, {"type": "t", "text": "3.0.co;2-b) PMID: "}, {"type": "a", "children": [{"type": "t", "text": "9462726"}], "href": "https://pubmed.ncbi.nlm.nih.gov/9462726"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Zhaoxia Ren, Pei-Yu Lin, Gordon K Klintworth, et al. 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