ArticleCancer biology & therapy2024
Mechanism investigation of Forsythoside A against esophageal squamous cell carcinoma
Article in Cancer biology & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Deguelin inhibits perineural invasion in esophageal squamous cell carcinoma via targeting BDNF/TrkB axis.Cancer biology & therapy · 2026Article
- Forsythiaside A inhibits progression and induces autophagy in lung adenocarcinoma: an integrated study combining network pharmacology and experimental validation.Scientific reports · 2026Article
- Forsythiaside A inhibits the progression of intrahepatic cholangiocarcinoma partially via suppressing oxidative stress-induced hepatic stellate cell activation and macrophage polarization.BMC biotechnology · 2026Article
- Anti-ovarian cancer effects of forsythiaside A: insights fromTranslational cancer research · 2025Article
- Artificial intelligence accelerates the identification of nature-derived potent LOXL2 inhibitors.Scientific reports · 2025Article
- Phytochemical profiling, antioxidant potential, and UHPLC-HRMS analysis of Phlomis genus aerial parts for therapeutic applications.Scientific reports · 2025Article
- Elucidating the Mechanisms of Astragalus Membranaceus in Colorectal Cancer Patients through Bioinformatics Analysis.Current medicinal chemistry · 2025Article
- Biomarkers of lymph node metastasis in esophageal cancer.Frontiers in immunology · 2024Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextForsythoside A (FSA) was extracted from Forsythia suspensa, a traditional Chinese medicine, which has been demonstrated to exert anti-inflammatory, antibacterial, and other pharmacological effects. However, the anticancer effect of FSA in esophageal squamous cell carcinoma (ESCC) has not been documented.
objectiveThe present study aimed to elucidate the mechanism of FSA against ESCC. MATERIALS AND
methodsNetwork pharmacology and molecular docking were employed to predict the mechanism. FSA was utilized to treat ESCC cell lines KYSE450 and KYSE30, followed by CCK-8 assay, cell cloning formation assay, flow cytometry, Western blot, RNA-seq analysis, and subsequent in vivo experiments.
resultsNetwork pharmacology and molecular docking predicted that the therapeutic effect of FSA in ESCC is mediated through proteins such as BCL2 and BAX, influencing KEGG pathways associated with apoptosis. In vitro experiments showed that FSA inhibited cell proliferation and plate clone formation, promoted cell apoptosis and impacted the cell cycle distribution of G2/M phase by regulating BCL2, BAX, and p21. Further RNA-seq in KYSE450 cells showed that FSA regulated the expression of 223 genes, specifically affecting the biological process of epidermal development. In vivo experiments showed that gastric administration of FSA resulted in notable reductions in both tumor volume and weight by regulating BCL2, BAX, and p21. 16S rRNA sequencing showed that FSA led to significant changes of beta diversity. Abundance of 11 specific bacterial taxa were considerably changed following administration of FSA.
conclusionsThis study presents a novel candidate drug against ESCC and establishes a foundation for future clinical application.
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