胰导管腺癌（PDAC）是全球最凶恶和致命的人类癌症之一，由于其高转移潜力，患有PDAC的患者预后较差，然而关于其高转移能力的潜在生物机制了解甚少。芩花素在治疗不同类型的癌症中具有显著的抗肿瘤功能。然而，芩花素对人类PDAC的治疗效果及其作用机制尚未被广泛了解。为了探索芩花素对抑制PDAC的转移能力在生物学特征、分子机制和潜在临床价值方面的作用，我们进行了几项体外、体内和体外研究。我们首先检查了芩花素对PDAC细胞转移能力的潜在调节作用。我们显示，芩花素能够显著抑制高度转移潜力的PDAC细胞在小鼠模型中的肝转移。我们采用高通量测序分析研究了芩花素在PDAC细胞中的生物学作用。我们发现，芩花素可能参与PDAC中的癌相关成纤维细胞（CAF）浸润。此外，我们根据TCGA数据库中的PDAC数据集，采用Cox分析建立了一个与芩花素相关的风险模型和一个长链非编码RNA（lncRNA）相关的模型，这表明了芩花素的临床价值。最后，我们揭示了芩花素在PDAC中的一个潜在下游靶点，我们认为芩花素可能通过FGFBP1促进CAF的浸润。因此，我们揭示了芩花素在调控PDAC肝转移中的新作用，这可能有助于其抗癌作用。我们提出，芩花素可能通过调节FGFBP1介导的CAF浸润来抑制PDAC的肝转移。我们的结果为芩花素的临床实用性提供了新的视角，并为抑制PDAC肝转移开辟了新的途径。Copyright © 2023 张，雷，周，钟，李，艾，郑，刘，朴，燕和赖。

Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant and lethal human cancers in the world due to its high metastatic potential, and patients with PDAC have a poor prognosis, yet quite little is understood regarding the underlying biological mechanisms of its high metastatic capacity. Baicalein has a dramatic anti-tumor function in the treatment of different types of cancer. However, the therapeutic effects of baicalein on human PDAC and its mechanisms of action have not been extensively understood. In order to explore the biological characteristic, molecular mechanisms, and potential clinical value of baicalein in inhibiting the metastatic capacity of PDAC. We performed several in vitro, in vivo, and in silico studies. We first examined the potential regulation of baicalein in the metastatic capacity of PDAC cells. We showed that baicalein could dramatically suppress liver metastasis of PDAC cells with highly metastatic potential in mice model. The high-throughput sequencing analysis was employed to explore the biological roles of baicalein in PDAC cells. We found that baicalein might be involved in the infiltration of Cancer-Associated Fibroblasts (CAF) in PDAC. Moreover, a baicalein-related risk model and a lncRNA-related model were built by Cox analysis according to the data set of PDAC from TCGA database which suggested a clinical value of baicalein. Finally, we revealed a potential downstream target of baicalein in PDAC, we proposed that baicalein might contribute to the infiltration of CAF via FGFBP1. Thus, we uncovered a novel role for baicalein in regulation of PDAC liver metastasis that may contribute to its anti-cancer effect. We proposed that baicalein might suppress PDAC liver metastasis via regulation of FGFBP1-mediated CAF infiltration. Our results provide a new perspective on clinical utility of baicalein and open new avenues for the inhibition of liver-metastasis of PDAC.Copyright © 2023 Zhang, Lei, Zhou, Zhong, Li, Ai, Zheng, Liu, Piao, Yan and Lai.