ArticleDiscover oncology2025
Sophocarpine inhibits the proliferation and induces apoptosis of glioblastoma cells through regulating the miR-21/PTEN/PI3K/AKT axis.
Article in Discover oncology, 2025. 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.
- Glioblastoma treatment patterns and outcomes over 18 years in an Irish cancer centre.Irish journal of medical science · 2026Article
- Sophocarpine alleviates chronic itch in mouse atopic dermatitis by inhibiting spinal astrocyte reactivity and pro-inflammatory signaling.Acta pharmacologica Sinica · 2026Article
- Exercise-associated microRNA programs as candidate modulators and biomarkers in glioblastoma: a narrative review.Discover oncology · 2026Review
- Alkaloids mediated regulation of microRNA in cancer: molecular insights and emerging therapeutic strategies.Frontiers in oncology · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
Sophocarpine (SC) has been reported to suppress tumorigenesis. But the effect of SC on glioblastoma (GBM) is unknown. This study explored the anti-proliferation and pro-apoptosis effects of SC on GBM cells and the molecular mechanism. Different concentrations of SC were used to treat human astrocyte NHA and GBM cells lines LN229 and SF539. CCK-8 was applied to analyze cell toxicity and proliferation. qRT-PCR and western blot were used to measure RNA and protein expressions, respectively. Cell cycle and cell apoptosis were determined by flow cytometry assay. The results indicated that SC inhibited proliferation and induced apoptosis of LN229 and SF539 cells in a dose-dependent manner. The arrest of the G0/G1 phase of GBM cells was increased after SC treatment. Moreover, SC downregulated miR-21 expression and upregulated PTEN expression in GBM cells. Overexpression of miR-21 partly abrogated the anti-proliferation and pro-apoptosis effects of SC on GBM cells, while exogenous PTEN partially eliminated the pro-proliferation and anti-apoptosis effects of miR-21 on GBM cells. Furthermore, SC treatment decreased the levels of PI3K/AKT pathway-related p-PI3K, p-AKT and PIP3 in GBM cells. The PI3K/AKT pathway activator 740Y-P partially reversed the reduced cell proliferation and enhanced cell apoptosis in SC-treated GBM cells. Significantly, we verified that SC suppressed the proliferation and enhanced apoptosis of GBM cells via inhibiting miR-21 while it was not entirely dependent on upregulation PTEN. Consequently, the potential mechanism of SC in induction apoptosis of GBM cells was verified, which might provide a new method for GBM treatment.
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