ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Sanggenol L Enhances Temozolomide Drug Sensitivity by Inhibiting Mitophagy and Inducing Apoptosis Through the Regulation of the TRIM16-OPTN Axis in Glioblastoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- TRIM16: a context-dependent E3 ligase in autophagy, oxidative stress, and immune regulation - from cancer and systemic disease.Frontiers in oncology · 2026Review
- Unraveling autophagy-metabolism crosstalk in cancer: Molecular insights and therapeutic strategies.Theranostics · 2026Review
- Sanggenol L Induces Endoplasmic Reticulum Stress and Triggers Cell Apoptosis in Glioblastoma by Binding to BiP.International journal of biological sciences · 2026Article
- Sanggenol L Enhances Temozolomide Drug Sensitivity by Inhibiting Mitophagy and Inducing Apoptosis Through the Regulation of the TRIM16-OPTN Axis in Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
12 authors.
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Abstract
Glioblastoma (GBM) is the most aggressive and lethal form of glioma, with current standard-of-care treatments including surgical resection, radiotherapy, and chemotherapy with temozolomide (TMZ). However, therapeutic resistance to TMZ frequently arises, partly attributed to autophagy, as demonstrated by analysis of clinical glioblastoma specimens. Through screening of mulberry metabolites, a bioactive small molecule, Sanggenol L (SL) is identified, which inhibits glioblastoma growth and blocks autophagy flux, thereby markedly enhancing TMZ chemosensitivity when delivered via a liposome-based system. Mechanistically, SL is found to suppress mitophagy by promoting ubiquitin-mediated proteasomal degradation of OPTN. Moreover, the first evidence that SL upregulates TRIM16 expression is presented, which acts as an E3 ubiquitin ligase for OPTN degradation in glioblastoma. TRIM16 depletion or OPTN overexpression partially abrogated SL-induced suppression of autophagy and apoptosis in GBM cells. Collectively, these findings suggest that SL enhances TMZ sensitivity by disrupting autophagy and inducing apoptosis through TRIM16-mediated OPTN degradation.
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