ArticleActa biochimica et biophysica Sinica2024
A network pharmacology- and transcriptomics-based investigation reveals an inhibitory role of β-sitosterol in glioma via the EGFR/MAPK signaling pathway.
Article in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- β-sitosterol suppresses malignant biological behaviors and glycolysis via modulating YBX1-hnRNP K interaction in non-small cell lung cancer.Scientific reports · 2026Article
- Anticancer Molecular Mechanisms of Phytosterols: An Updated Review on Clinical Trials.Food science & nutrition · 2026Review
- Mechanism of β‑sitosterol in treating keloids: Network pharmacology, molecular docking and experimental verification.Molecular medicine reports · 2025Article
- β-Sitosterol Mitigates Apoptosis, Oxidative Stress and Inflammatory Response by Inactivating TLR4/NF-кB Pathway in Cell Models of Diabetic Nephropathy.Cell biochemistry and biophysics · 2025Article
- β-sitosterol suppresses fibroblast growth factor and epidermal growth factor receptors to induce apoptosis and inhibit migration in lung cancer: an in vitro study.American journal of cancer research · 2025Article
- Mechanism of Smilax china L. in the treatment of intrauterine adhesions based on network pharmacology, molecular docking and experimental validation.BMC complementary medicine and therapies · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
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Abstract
Glioma is characterized by rapid cell proliferation, aggressive invasion, altered apoptosis and a poor prognosis. β-Sitosterol, a kind of phytosterol, has been shown to possess anticancer activities. Our current study aims to investigate the effects of β-sitosterol on gliomas and reveal the underlying mechanisms. Our results show that β-sitosterol effectively inhibits the growth of U87 cells by inhibiting proliferation and inducing G2/M phase arrest and apoptosis. In addition, β-sitosterol inhibits migration by downregulating markers of epithelial-mesenchymal transition (EMT). Mechanistically, network pharmacology and transcriptomics approaches illustrate that the EGFR/MAPK signaling pathway may be responsible for the inhibitory effect of β-sitosterol on glioma. Afterward, the results show that β-sitosterol effectively suppresses the EGFR/MAPK signaling pathway. Moreover, β-sitosterol significantly inhibits tumor growth in a U87 xenograft nude mouse model. β-Sitosterol inhibits U87 cell proliferation and migration and induces apoptosis and cell cycle arrest in U87 cells by blocking the EGFR/MAPK signaling pathway. These results suggest that β-sitosterol may be a promising therapeutic agent for the treatment of glioma.
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