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https://www.selleckchem.com/products/inaxaplin.html https://www.selleckchem.com/products/inaxaplin.html Clinical study standard protocol: PRednisolone in early soften cutaneous Endemic Sclerosis (PRedSS). Bioinformatic and Western blot analyses showed that CLDN8 suppressed proliferation, migration, and invasion of 786-O ccRCC cells through the epithelial-mesenchymal transition and AKT pathways. CLDN8 could serve as an independent prognostic factor in ccRCC, in which it suppresses 786-O proliferation, migration, and invasion through EMT and AKT pathways. CLDN8 could serve as an independent prognostic factor in ccRCC, in which it suppresses 786-O proliferation, migration, and invasion through EMT and AKT pathways. Peroxiredoxin 1 (PRDX1) has been identified as a dual regulator of tumorigenesis. However, its expression, clinical significance, and biological function in nasopharyngeal carcinoma (NPC) remain unknown. This study aimed to explore the role and underlying mechanisms of PRDX1 in NPC. The expression of PRDX1 in NPC tissues was evaluated by immunohistochemistry, and the relationships between the expression of PRDX1 and clinical features and prognosis of NPC patients were analyzed. The effects of PRDX1 on NPC cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) were examined. A tumor-bearing model of nude mouse was established to verify the function of PRDX1 in vivo. PRDX1 expression level was negatively associated with recurrence and metastasis of NPC. PRDX1 knockdown promoted NPC cell proliferation, migration, invasion and EMT in vitro, and enhanced tumor growth in vivo, while PRDX1 overexpression had opposite effects. Furthermore, transcriptome analysis showed that PRDX1 inhibited the activation of PI3K/AKT/TRAF1 signaling in NPC cells. PRDX1 inhibits NPC by inhibiting the activation of PI3K/AKT/TRAF1 signaling. PRDX1 is a tumor suppressor in human NPC and may be a prognostic biomarker for NPC patients. PRDX1 inhibits NPC by

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