ArticleCytotechnology2025
Astragalus polysaccharide regulates the cervical cancer cell cycle and inhibits cisplatin resistance by blocking the Wnt/β-catenin pathway through the PPARD/CDC20 axis.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Astragalus polysaccharides combined with radiochemotherapy for cervical cancer: a systematic review and meta-analysis of randomized controlled studies.Frontiers in pharmacology · 2025Pooled it
- Mechanistic insights into the roles of astragalosides andOncology reports · 2026Review
- Natural polysaccharides as multifunctional anti-cancer agents: structure-activity relationships, mechanisms of action, and therapeutic potential.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astragalus polysaccharide (APS) can prevent tumor progression and cisplatin resistance. This paper investigates the downstream mechanism of APS in regulating cervical cancer (CC) cisplatin resistance. Cisplatin-resistant CC cell lines were constructed. APS inhibited the proliferation of Hela/DDP and SiHa/DDP cells and increased apoptosis. The downstream transcription factors of APS and the downstream targets of the transcription factor PPARD were predicted using bioinformatics tools. PPARD and CDC20 levels were detected in parental and drug-resistant cell lines. CC cells were treated with APS or a combined knockdown of PPARD and CDC20, or a Wnt/β-catenin pathway agonist, and the proliferation, cell cycle distribution, and apoptosis were examined. A xenograft tumor model was constructed to monitor tumor growth under cisplatin treatment. APS promoted PPARD expression, and PPARD knockdown reduced apoptosis. PPARD transcriptionally repressed CDC20 by binding to its promoter and CDC20 downregulation hindered the proliferation of cisplatin-resistant CC cells and increased the apoptotic rate. Wnt/β-catenin pathway agonist annulled the ameliorative effect of CDC20 knockdown on CC cell growth. CDC20 overexpression reversed the hindered tumor growth by APS treatment. Overall, APS inhibits CC progression and cisplatin resistance by promoting PPARD and suppressing CDC20 transcription to inhibit the Wnt/β-catenin pathway. Supplementary Information: The online version contains supplementary material available at 10.1007/s10616-025-00785-9.
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