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<p>Pancreatic cancer is one of the deadliest cancers in the world. Phytochemicals are considered as potential anticancer drugs because of their safety and low cost. Sodium new houttuyfonate (SNH) is derived from Houttuynia cordata Thunb. (HCT), which is a famous edible and medicinal plant in China. Although research findings suggest that SNH possesses anticancer properties, its role and mechanisms in pancreatic cancer remain unclear. Using network pharmacology, we identified 49 potential targets of SNH action in pancreatic cancer. In vitro, we confirmed that SNH inhibited the proliferation and invasion, promoted mitochondrial damage and induce apoptosis of PANC-1 cells. In vivo, SNH promoted tumor apoptosis and inhibited pancreatic cancer development in mice. In addition, RNA sequencing demonstrated that SNH exerted anticancer effects by regulating the MAPK (Mitogen-activated protein kinase) signaling pathway and identified FGF1 (Fibroblast growth factor 1) as a key gene in this process. Moreover, FGF1 is also an important gene affecting tumor angiogenesis, which is an important process in tumor development. Therefore, the study demonstrated that SNH inhibited pancreatic cancer progression by down-regulating FGF1 expression and inactivating the p38/MAPK pathway, thereby affecting tumor angiogenesis. Our study provides a potentially effective strategy for the treatment of pancreatic cancer.</p>

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Sodium new houttuyfonate affects tumor angiogenesis by suppressing FGF1 expression and the p38/MAPK signaling pathway in pancreatic cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月15日

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  • Xin Yu,
  • Lihong Jiang,
  • Xiaoyu Yang

摘要

Pancreatic cancer is one of the deadliest cancers in the world. Phytochemicals are considered as potential anticancer drugs because of their safety and low cost. Sodium new houttuyfonate (SNH) is derived from Houttuynia cordata Thunb. (HCT), which is a famous edible and medicinal plant in China. Although research findings suggest that SNH possesses anticancer properties, its role and mechanisms in pancreatic cancer remain unclear. Using network pharmacology, we identified 49 potential targets of SNH action in pancreatic cancer. In vitro, we confirmed that SNH inhibited the proliferation and invasion, promoted mitochondrial damage and induce apoptosis of PANC-1 cells. In vivo, SNH promoted tumor apoptosis and inhibited pancreatic cancer development in mice. In addition, RNA sequencing demonstrated that SNH exerted anticancer effects by regulating the MAPK (Mitogen-activated protein kinase) signaling pathway and identified FGF1 (Fibroblast growth factor 1) as a key gene in this process. Moreover, FGF1 is also an important gene affecting tumor angiogenesis, which is an important process in tumor development. Therefore, the study demonstrated that SNH inhibited pancreatic cancer progression by down-regulating FGF1 expression and inactivating the p38/MAPK pathway, thereby affecting tumor angiogenesis. Our study provides a potentially effective strategy for the treatment of pancreatic cancer.