ArticleFrontiers in pharmacology2024
Maslinic acid induces autophagy and ferroptosis via transcriptomic and metabolomic reprogramming in prostate cancer cells.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- NCOA4-driven ferritinophagy and GSH reprogramming underlie maslinic acid-induced ferroptosis and autophagy in breast cancer.Translational cancer research · 2026Article
- Targeting Hsp70 triggers ferroptosis: a novel anti-cancer mechanism of a marine natural product in prostate cancer.Natural products and bioprospecting · 2026Article
- Interaction between Maslinic acid and HSF1 enhances the ubiquitin degradation of HSF1, resulting in the inhibitory effect of pancreatic cancer.Discover oncology · 2025Article
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Authors and funding
17 authors.
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Abstract
Prostate cancer has the second highest incidence among male malignancies. Only a few studies exist on the inhibitory effects of maslinic acid (MA) on prostate cancer. Herein we found that MA inhibits prostate cancer cell proliferation by decreasing CDK2, CDK4, and CDK6 expression and concurrently increasing p27, Rb, p-Rb expression. Further, MA was observed to induce prostate cancer cell autophagy by increasing the expression of p53, p-p53, ULK1, Beclin1, Atg7, and Atg5 and the ratio of LC3-II/I and concurrently decreasing the expression of ERK1/2 and mTOR. In addition, MA induced RM-1 cell ferroptosis by regulating glutathione, glutamate, and oxidized glutathione concentrations, inhibiting
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