ArticleScientific reports2023
Taraxasterol suppresses the proliferation and tumor growth of androgen-independent prostate cancer cells through the FGFR2-PI3K/AKT signaling pathway.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Knockdown of ALOX15 alleviates acute coronary syndrome via the FGFR2/PI3K/AKT signaling pathway.Biomedical reports · 2026Article
- Curcumol attenuates hyperproliferation and inflammatory response in a psoriatic HaCaT keratinocyte model by inhibiting the PI3K-Akt pathway and ameliorates skin lesions and inflammatory status in psoriasis-like mice.Inflammopharmacology · 2025Article
- Taraxasterol mediated autophagy inhibition in pancreatic encephalopathy involves its regulation on L1 cell adhesion molecule.Cytotechnology · 2025Article
- Botany, Traditional Use, Phytochemistry, Pharmacology and Quality Control ofPharmaceuticals (Basel, Switzerland) · 2024Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PCa) is prevalent among older men and difficult to survive after metastasis. It is urgent to find new drugs and treatments. Several studies show that taraxasterol (TAX) has important anti-inflammatory, anti-oxidative and anti-tumor effects. However, the function and mechanisms of TAX in PCa remain unclear. Here, we found that TAX could significantly suppress the viability and growth of androgen-independent PCa cells and down-regulate the expression of c-Myc and cyclin D1 in vitro. Mechanistically, PI3K/AKT signaling pathway was weakened and the expression of FGFR2 was reduced after TAX treatment in androgen-independent PCa cells. Moreover, TAX evidently inhibited the tumor growth in nude mice and the expression of c-Myc, cyclin D1, p-AKT and FGFR2 were down-regulated in xenograft tumor. These results indicate that TAX suppresses the proliferation of androgen-independent PCa cells via inhibiting the activation of PI3K/AKT signaling pathway and the expression of FGFR2, which means TAX may be a novel anti-tumor agent for later PCa treatment.
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