ArticleBiochemistry and biophysics reports2022
Saikosaponin D improves chemosensitivity of glioblastoma by reducing the its stemness maintenance.
Article in Biochemistry and biophysics reports, 2022. 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.
- Traditional Chinese Medicine-Derived Active Ingredient and Formulation Therapy for Glioma: Multi-Target Mechanisms, Drug Delivery Systems, and Advances in Clinical Translational Research.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Saikosaponin D overcomes gemcitabine resistance in pancreatic cancer via AKT/mTOR pathway inhibition and synergistic induction of apoptosis and autophagy.Oncology reports · 2026Article
- Research progress on the molecular mechanisms of Saikosaponin D in various diseases (Review).International journal of molecular medicine · 2025Review
- Advances in the anti-tumor mechanisms of saikosaponin D.Pharmacological reports : PR · 2024Review
- Saikosaponin D reverses epinephrine- and norepinephrine-induced gemcitabine resistance in intrahepatic cholangiocarcinoma by downregulating ADRB2/glycolysis signaling.Acta biochimica et biophysica Sinica · 2023Article
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7 authors.
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Abstract
Objective: Chemotherapy is one of the important adjuvant methods for the treatment of glioblastoma (GBM), and chemotherapy resistance is a clinical problem that neurooncologists need to solve urgently. It is reported that Saikosaponin D (SSD), an active component of Methods: The CCK8 assay, Wound healing assay and Matrigel invasion assay were used to detect the effect of SSD on the phenotype of GBM cells. We detected the effect of SSD on the chemosensitivity of GSM by Flow cytometry, LDH content and MTT assay. Then, we used cell plate cloning, semi-quantitative PCR and western blotting experiments to detect the effect of SSD on the stem potential of GBM cells. Finally, the effect of SSD on the chemosensitivity of GBM and its potential mechanism were verified by nude mouse experiments in vivo Results: firstly, we found that SSD could partially inhibit the malignant phenotype of LN-229 cells, including inhibiting migration, invasion and apoptosis, and increasing the apoptosis rate and lactate dehydrogenase (LDH) release of LN-229 cells under the treatment of temozolomide (TMZ), that is to say, increasing the chemotherapy effect of TMZ on the cells. In addition, we unexpectedly found that SSD could partially inhibit the colony forming ability of LN-229 cells, which directly related to the stemness maintenance potential of cancer stem cells. Subsequently, our results showed that SSD could inhibit the gene and protein expression of stemness factors (OCT4, SOX2, c-Myc and Klf4) in LN-229 cells. Finally, we verified that SSD could improve the chemotherapy effect of TMZ by inhibiting the stem potential of glioblastoma in vivo nude mice. Conclusion: this research can provide a certain theoretical basis for the application of SSD in the chemotherapy resistance of GBM and its mechanism of action, and provide a new hope for the clinical treatment of glioblastoma.
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