ArticleScientific reports2025
Sciellin inhibits senescence and promotes pancreatic cancer progress by activating the notch signaling pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Spatially-resolved subtype progression reveals metabolic vulnerabilities in pancreatic ductal adenocarcinoma.Molecular cancer · 2026Article
- Comprehensive Exploration of NOTCH2NLA Across Cancers and Its Potential Roles in Prognosis and Immune System Interactions.Current medicinal chemistry · 2026Article
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7 authors.
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Abstract
Pancreatic cancer (PC) incidence is increasing annually globally, and the five-year survival rate of patients with PC is approximately 10%. Cellular senescence is a regulatory mechanism against cancer that prevents tumor development by inhibiting the proliferation of damaged or abnormal cells. However, the mechanisms underlying cellular senescence in PC is unclear. Sciellin (SCEL) is a precursor protein of the cornified envelope predominantly enriched in epithelial cells. Previous studies have discovered potential links between SCEL and cellular senescence through bioinformatics analysis. Therefore, the specific role of SCEL in cellular senescence and the malignant features of PC are unclear. In vivo and in vitro assays were performed to investigate the role of SCEL in PC cell senescence, proliferation, invasion, and metastasis. Gene set enrichment analysis was used to identify the Notch signaling pathways activated by SCEL, and coimmunoprecipitation was used to detect proteins that interact with SCEL. The results revealed that SCEL was significantly upregulated in PC tissues and cell models and was correlated with poor clinical outcomes. Further investigation revealed that the interaction between SCEL and Jagged-1 promotes the activation of the Notch signaling pathway, effectively inhibiting the senescence of PC cells while enhancing their proliferation, invasion, and metastatic capabilities. Therefore, SCEL is a potential therapeutic target for PC.
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