Hederagenin suppresses glioma cell biological activities via Nur77 in vitro study
Yuxiang Dai1, Ngarmbaye Masra1, Lu Zhou1
1Department of Neurosurgery, Nanjing Drum Tower Hospital The Affiliated Hospital of Nanjing University Medical School Nanjing China.
Abstract:
The aim of this research was to discuss Hederagenin's antitumor effects on glioma by in vitro study. U251 and U87 cell lines were used as research target in our research. In the first step, the different Hed concentrations were treated to U251 and U87 cell lines, and the second step is Nur77 transfection in U251 and U87 with Hed treatment; measuring cell proliferation by MTT and EdU staining; evaluating cell invasion and migration abilities by transwell assay and relative gene and protein expressions by RT-qPCR and WB assay. Compared with NC group, U251 and U87 cell proliferation were significantly depressed with cell apoptosis significantly increasing, and cell invasion and migration abilities were significantly inhibited in Hed-treated groups (p < .05, respectively); however, with Nur77 transfection, the Hed's antitumor effects disappeared. Meanwhile, with Hed supplement, Nur77, PI3K, and AKT gene expressions were significantly downregulated (p < .05, respectively) in Hed-treated groups; and Nur77, p-PI3K, and p-AKT protein expressions were significantly decreased (p < .05, respectively) in Hed-treated groups. Hed had antitumor effects on glioma cell biological activities via Nur77/PI3K/AKT pathway in vitro study.
Insights
Hederagenin demonstrates antitumor effects against glioma cells by inhibiting proliferation and invasion. These effects are mediated through the Nur77/PI3K/AKT pathway, as blocking Nur77 diminishes Hederagenin
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Glioblastoma (GBM) is an aggressive brain tumor with limited treatment options.
- Natural compounds are being investigated for their potential anticancer properties.
Purpose of the Study:
- To investigate the in vitro antitumor effects of Hederagenin (Hed) on human glioblastoma cell lines (U251 and U87).
- To elucidate the underlying molecular mechanisms, particularly the role of the Nur77/PI3K/AKT pathway.
Main Methods:
- Cell proliferation was assessed using MTT and EdU staining assays.
- Cell invasion and migration were evaluated using Transwell assays.
- Gene and protein expression levels of Nur77, PI3K, and AKT were measured by RT-qPCR and Western Blot (WB).
Main Results:
- Hederagenin significantly inhibited glioblastoma cell proliferation and induced apoptosis.
- Hederagenin treatment significantly reduced cell invasion and migration capabilities.
- Nur77 transfection abrogated the antitumor effects of Hederagenin, indicating its crucial role.
- Hederagenin downregulated the gene expression of Nur77, PI3K, and AKT, and protein expression of Nur77, p-PI3K, and p-AKT.
Conclusions:
- Hederagenin exhibits significant in vitro antitumor activity against glioblastoma.
- The antitumor effects of Hederagenin are mediated via the Nur77/PI3K/AKT signaling pathway.
- Hederagenin represents a potential therapeutic agent for glioblastoma treatment.
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