ArticleJournal of molecular histology2025
Neferine induces cell growth inhibition and apoptosis via ROS-mediated activation of p38 in pancreatic ductal adenocarcinoma cells.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Neferine-Targeted Inhibition of TrxR1 Triggers Apoptosis Through Disrupting Redox Homeostasis in Pancreatic Cancer Cells.Molecular carcinogenesis · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Pancreatic cancer is a lethal malignancy with limited effective treatment options available. Neferine, an alkaloid derived from the seed embryos of lotus, has been reported to exert tumor suppressive functions in multiple cancer types, but its exact roles in pancreatic ductal adenocarcinoma (PDAC) and the underlying mechanisms remain largely elusive. In this study, cell counting kit-8, clone formation, 5-ethynyl-2′-deoxyuridine and TdT-mediated dUTP Nick-End Labeling staining, and flow cytometry assays were employed to evaluate the anti-tumor effect of neferine against PDAC. Western blotting was performed to analyze the related protein expression. We demonstrated that neferine reduced cellular proliferation and triggered mitochondrial-dependent apoptosis in PDAC cells. Meanwhile, neferine treatment induced the generation of reactive oxygen species (ROS) and p38 activation. Notably, the inhibition of ROS generation and p-p38 expression attenuated the anticancer effects of neferine. In conclusion, ROS-induced p38 activation contributes to the cell growth inhibition of neferine in PDAC cells.
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