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• W3200948612 abstract "Abstract Oxysterol-binding protein 2 (OSBP2) is crucial for the promotion of growth and development of cancers, however, its effects in pancreatic ductal adenocarcinoma (PDAC) were still unclear. Here we report the evidence that OSBP2 works as an efficient tumor-associated protein to lead to PDAC extremely malignant characters. We discovered that raised OSBP2 expression in primary tumors was associated with shorter survival in PDAC patients. Therefore, we used immunohistochemistry to analysis the levels of OSBP2 expression in PDAC tissues and adjacent para-cancer tissues. We used wound-healing assay and transwell assay to evaluate the effects of OSBP2 on PDAC cells’ (ASPC-1 and BXPC-3) migration and invasion, respectively. Using CCK-8 and Annexin V / PI double staining, we evaluated the effects of OSBP2 on PDAC cells’ proliferation and apoptosis, respectively. We also explored the effect of OSBP2 on chemosensitivity (gemcitabine and 5-Fluorouracil). And we further validated these findings in vivo of mice. At last, we used western blot to analysis the effect of OSBP2 on PDAC cells’ phenotype. We proved that OSBP2 overexpression promoted PDAC cells’ migration, invasion, proliferation and chemotherapy resistance, decreased apoptosis. OSBP2 overexpression downregulated E-cadherin, and upregulated the levels of N-cadherin, vimentin, Snail, Slug, ZEB1 and β-Catenin. Taken collectively, our findings indicated that OSBP2 exhibited overexpression in PDAC, and upregulation of OSBP2 may promote the progression of PDAC. OSBP2 may have potential diagnostic and therapeutic values in PDAC." @default.
• W3200948612 created "2021-09-27" @default.
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• W3200948612 date "2021-09-09" @default.
• W3200948612 modified "2023-09-23" @default.
• W3200948612 title "Oxysterol-Binding Protein 2 Promotes Pancreatic Ductal Adenocarcinoma Progression Through Epithelial-Mesenchymal Transition Process" @default.
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• W3200948612 doi "https://doi.org/10.21203/rs.3.rs-832603/v1" @default.
• W3200948612 hasPublicationYear "2021" @default.
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