ArticleBioFactors (Oxford, England)
OSBPL10-CNBP axis mediates hypoxia-induced pancreatic cancer development.
Article in BioFactors (Oxford, England). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Identification and validation of BLK and OSBPL10 as diagnostic and prognostic biomarkers for nasopharyngeal carcinoma through machine learning algorithms.Scientific reports · 2026Article
- A new candidate tumor suppressor tRF-Ser inhibits gastric cancer progression by regulating the CNBP/HSPA8 axis.Cell death & disease · 2026Article
- Role of Oxysterol-Binding Protein Family in Cholesterol Metabolism and Cancer Progression: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- OSBPL3-driven sterol metabolic reprogramming promotes oncogenic signaling and therapeutic resistance in pancreatic cancer.Theranostics · 2026Article
- Recent advances in hydrogel-based delivery systems for the treatment of pancreatic cancer.Materials today. Bio · 2025Review
- Potential prognostic biomarker of OSBPL10 in pan-cancer associated with immune infiltration.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- OSBPL10-CNBP axis mediates hypoxia-induced pancreatic cancer development.BioFactors (Oxford, England)Article
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7 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of malignancies with worst outcomes among digestive system tumors. Identification of novel biomarkers is of great significance for treatment researches and prognosis prediction of pancreatic cancer patients. Due to OSBPL10 known involvement in oncogenic activity in other tumors, we elucidated the mechanism underlying its contribution to pancreatic cancer progression. We employed data from the Gene Expression Omnibus database to detect the expression of OSBPL10 in normal and pancreatic cancer tissues. A series of assays were conducted to assess the impact of OSBPL10 on the proliferation and metastatic capacities of pancreatic cancer cells and the influence of OSBPL10 on macrophages were evaluated by Flow cytometry. In addition, Co-immunoprecipitation, mass spectrometry, and western blot assays were utilized to investigate the potential mechanisms of OSBPL10 activity. From our study, OSBPL10 is revealed to be upregulated in pancreatic cancer, with poor prognosis. The overexpression promotes malignant behaviors of pancreatic cancer cells and has an impact on tumor immune microenvironment by stimulating the transformation M1 macrophages into M2 macrophages. Mechanistically, hypoxia induces the expression of OSBPL10 through interaction between hypoxia-inducible factor 1-α and the promoter region of OSBPL10. Additionally, OSBPL10 directly bound to CNBP, mediating CNBP expression and ultimately regulating the proliferation and metastasis capacity of pancreatic cancer cells, as well as influencing macrophage polarization. The research emphasized the oncogenic role of OSBPL10 in pancreatic cancer, uncovering key mechanisms involving hypoxia, HIF-1α, and CNBP. The finding suggests that OSBPL10 is a novel biomarker in pancreatic cancer, making it a potential therapeutic target for intervention in this malignancy.
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