4.7 Article

Herba Patriniae and its component Isovitexin show anti-colorectal cancer effects by inducing apoptosis and cell-cycle arrest via p53 activation

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 168, Issue -, Pages -

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2023.115690

Keywords

Herba Patriniae; Cell Cycle; Isovitexin Colorectal Cancer; p53 pathway; ,Apoptosis

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This study investigated the potential mechanisms of Herba Patriniae (HP) and its primary component Isovitexin against colorectal cancer (CRC) using network pharmacology analysis and in vitro and in vivo experiments. The study identified nine bioactive compounds of HP and predicted 3460 CRC-related targets. Ten hub genes, including CDK4, CDK2, CDK1, CCND1, CCNB1, CCNA2, MYC, E2F1, CHEK1, and CDKN1A, were identified as core target genes. The study also found that HP activated the p53 signaling pathway, promoting apoptosis and suppressing cell proliferation. This study provides valuable insights into the underlying mechanisms of HP and its component Isovitexin against CRC, supporting further experimental verification of their clinical application.
Colorectal cancer (CRC) is the most prevalent cancer of the digestive tract. Herba Patriniae (also known as Bai Jiang Cao, HP) have been widely used to manage diarrhea, ulcerative colitis, and several cancers, including CRC. Nonetheless, the molecular mechanisms underlying the pharmacological action of HP on CRC remain unclear. This study investigated the underlying mechanisms of HP against CRC using network pharmacology analysis and in vitro and in vivo experiments. The results revealed nine bioactive compounds of HP. Furthermore, 3460 CRCrelated targets of the identified active compounds were predicted from the Gene Expression Omnibus (GEO) database. Furthermore, 65 common targets were identified through the intersection of two related targets. Moreover, ten hub genes, including CDK4, CDK2, CDK1, CCND1, CCNB1, CCNA2, MYC, E2F1, CHEK1, and CDKN1A were identified through the topological analysis. Meanwhile, the GO and KEGG pathway analysis revealed that the core target genes were majorly enriched in the p53 and HIF-1 signaling pathways. Moreover, HP promoted apoptosis and suppressed cell proliferation by activating the p53 signaling pathway in a dosedependent manner, while a similar effect was observed for Isovitexin (the primary component of HP). Overall, this study provides valuable insights into the underlying mechanisms of HP and its component Isovitexin against CRC, providing a theoretical foundation for additional experimental verification of its clinical application.

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