ArticleOncoTargets and therapy2020
Polyphyllin VI Induces Apoptosis and Autophagy via Reactive Oxygen Species Mediated JNK and P38 Activation in Glioma.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
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- Identification and vitro verification of the potential drug targets of active ingredients of Chonglou in the treatment of lung adenocarcinoma based on EMT-related genes.Frontiers in genetics · 2023Article
- Polyphyllin II induced apoptosis of NSCLC cells by inhibiting autophagy through the mTOR pathway.Pharmaceutical biology · 2022Article
- Bioactive secondary metabolites inHeliyon · 2022Review
- Potential targets and treatments affect oxidative stress in gliomas: An overview of molecular mechanisms.Frontiers in pharmacology · 2022Review
- The functional role of p38 MAPK pathway in malignant brain tumors.Frontiers in pharmacology · 2022Review
- Machine learning and bioinformatics-based insights into the potential targets of saponins inFrontiers in genetics · 2022Article
- Phlorizin from sweet tea inhibits the progress of esophageal cancer by antagonizing the JAK2/STAT3 signaling pathway.Oncology reports · 2021Article
- High Adenosine Extracellular Levels Induce Glioblastoma Aggressive Traits Modulating the Mesenchymal Stromal Cell Secretome.International journal of molecular sciences · 2020Article
- Neferine induces apoptosis by modulating the ROS‑mediated JNK pathway in esophageal squamous cell carcinoma.Oncology reports · 2020Article
- Genetic and Clinical Characterization of HOXB2 in Glioma.OncoTargets and therapy · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPolyphyllin VI (PPVI), a bioactive component derived from a traditional Chinese herb
methodsFive glioma cell lines (U251, U343, LN229, U87 and HEB) and an animal model were employed in the study. Anti-proliferation effects of PPVI were first determined using CCK-8 cell proliferation and clone formation assays, then reactive oxygen species (ROS), cell cycle progression and apoptosis effects measured by flow cytometry. The effect of PPVI on protein expression was quantified by Western blot analysis.
resultsData showed that PPVI inhibited the proliferation of glioma cell lines by modulating the G2/M phase. Additionally, incubation of cells with PPVI promoted apoptosis, autophagy, increased accumulation of ROS and activated ROS-modulated JNK and p38 pathways. On the other hand, N-acetyl cysteine, a ROS inhibitor, attenuated PPVI-triggered effects. Furthermore, JNK and p38 inhibitors ameliorated PPVI-triggered autophagy and apoptosis in glioma cells. In vivo assays showed that PPVI inhibited tumor growth of U87 cell line in nude mice.
conclusionOverall, these data suggested that PPVI might be an effective therapeutic agent for glioma.
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