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Tumor protein D52-like 2 (TPD52L2) is a coiled-coil domain protein highly expressed in many tissues, with especially high abundance in cancer cells, such as HeLa cells[1][2][4]. TPD52L2 localizes to small intracellular transport vesicles (nanovesicles) and regulates protein trafficking and recycling, affecting Golgi integrity and cargo movement[1][2]. Functionally, it promotes cell proliferation, migration, and invasion, and its expression levels correlate with prognosis in cancers such as breast cancer and glioblastoma[2][3][4][6]. TPD52L2 modulates cellular heterogeneity, influences the epithelial–mesenchymal transition (EMT) via β-catenin and Snail pathways, and is implicated in regulating the tumor microenvironment (TME)[3][6]. Knockdown or inhibition of TPD52L2 reduces tumor cell proliferation, induces apoptosis, and sensitizes cells to chemotherapy[3][4]. Its transcript variant V6 is particularly oncogenic and is a strong candidate for targeted therapies or predictive biomarkers[2][6].
Gene knockdown (e.g., siRNA, shRNA): inhibits cell proliferation and migration, promotes apoptosis\nmicroRNA inhibition (miR-217 reduces TPD52L2 expression, impairing cancer cell growth)
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