Institute of Paulownia, Henan Agricultural University, Zhengzhou, Henan 450002, PR China; School of Life Science and Engineering, Henan University of Urban Construction, Pingdingshan, Henan 467044, PR China.
School of Life Science and Engineering, Henan University of Urban Construction, Pingdingshan, Henan 467044, PR China; College of Life Science, Yangtze University, Jingzhou, Hubei 434023, PR China.
Int J Biol Macromol. 2024 Jan;254(Pt 1):127627. doi: 10.1016/j.ijbiomac.2023.127627. Epub 2023 Oct 24.
To develop an inhibitor targeting the Wnt/β-catenin signaling pathway, flavonoid monomer that can interact with β-catenin was isolated from Paulownia flowers. Luteolin may form stable hydrogen bonds with β-catenin by molecular docking. Fluorescence quenching analysis determined the physical interaction between luteolin and β-catenin. The binding of luteolin to β-catenin caused a loss of α-helical structure and induced a conformational change through circular dichroism spectroscopy. Luteolin inhibits the activity of the Wnt signaling, causing cholangiocarcinoma (CCA) cell cycle arrest in the G2/M phase, leading to cell apoptosis and inhibition of cell migration. In addition, transcriptome and proteomics analysis showed that the differentially expressed proteins were significantly enriched in the Wnt/β-catenin pathway. β-catenin protein in the nucleus was significantly decreased, while C-Myc and cyclin D1 in the CCA cells were significantly decreased after luteolin treatment. Additionally, activation of the Wnt/β-catenin signaling reversed the inhibitory effect of luteolin on the migration of CCA cells. Therefore, luteolin can directly interact with β-catenin and act as an inhibitor of β-catenin, inhibiting proliferation and reducing the migration ability of CCA cells by inhibiting the Wnt/β-catenin pathway. This study provides a scientific basis for the development of Wnt/β-catenin pathway inhibitors and the prevention and treatment of CCA.
为了开发针对 Wnt/β-catenin 信号通路的抑制剂,从泡桐花中分离出一种可以与β-catenin 相互作用的黄酮单体。通过分子对接,木犀草素可能与β-catenin 形成稳定的氢键。荧光猝灭分析确定了木犀草素与β-catenin 之间的物理相互作用。木犀草素与β-catenin 的结合导致α-螺旋结构丧失,并通过圆二色性光谱诱导构象变化。木犀草素抑制 Wnt 信号通路的活性,导致胆管癌细胞周期停滞在 G2/M 期,引起细胞凋亡和抑制细胞迁移。此外,转录组和蛋白质组学分析表明,差异表达的蛋白质在 Wnt/β-catenin 通路中显著富集。木犀草素处理后,CCA 细胞中核内β-catenin 蛋白明显减少,而 C-Myc 和 cyclin D1 明显减少。此外,Wnt/β-catenin 信号的激活逆转了木犀草素对 CCA 细胞迁移的抑制作用。因此,木犀草素可以直接与β-catenin 相互作用,作为β-catenin 的抑制剂,通过抑制 Wnt/β-catenin 通路抑制 CCA 细胞的增殖和降低迁移能力。本研究为开发 Wnt/β-catenin 通路抑制剂和预防与治疗 CCA 提供了科学依据。