ArticleFrontiers in pharmacology2026
Isoalantolactone inhibits pancreatic ductal adenocarcinoma progression via direct targeting of NLRP3-mediated inflammation-angiogenesis axis.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) is the fifth most common malignancy globally, with tumor uncontrolled angiogenesis being major causes of therapeutic failure and patient death. Isoalantolactone (IATL), a natural compound, exhibits antioxidant, anti-inflammatory, anti-proliferative, and anti-tumor properties. However, its role in inhibiting tumor angiogenesis in pancreatic cancer and the underlying mechanisms remain unclear. This study aims to investigate the anti-angiogenic effects of IATL in PDAC and elucidate the associated molecular pathways. Methods: Results: IATL significantly inhibited the proliferation and migration of Panc02, PANC-1, and SW1990 cells. In the orthotopic pancreatic cancer model, IATL dose-dependently suppressed tumor growth, as evidenced by reduced IVIS fluorescence signals and tumor volume. IATL also markedly inhibited angiogenesis, as shown by reduced HUVECs migration and tube formation, decreased tumor blood perfusion detected by laser speckle imaging, and downregulated CD34 and VEGFA expression both Conclusion: IATL functions as a novel NLRP3 pathway inhibitor, suppressing angiogenesis through anti-inflammatory mechanisms, thereby effectively inhibiting PDAC progression. These findings suggest that IATL holds potential as a therapeutic agent for pancreatic cancer.
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