ArticleMolecular medicine reports2020
Tubeimoside‑1 induces apoptosis in human glioma U251 cells by suppressing PI3K/Akt‑mediated signaling pathways.
Article in Molecular medicine reports, 2020. 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, 9 citations in OpenAlex.
- FANCI is involved in the malignant progression of glioma cells by regulating the Akt/Bcl-2 signaling pathway.Discover oncology · 2025Article
- Piezo1-related physiological and pathological processes in glioblastoma.Frontiers in cell and developmental biology · 2025Review
- PCGF1 is a prognostic biomarker and correlates with tumor immunity in gliomas.Annals of translational medicine · 2022Article
- Tubeimoside-1: A review of its antitumor effects, pharmacokinetics, toxicity, and targeting preparations.Frontiers in pharmacology · 2022Review
- Chinese endemic medicinal plantFrontiers in pharmacology · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubeimoside-1 (TBMS1), a traditional Chinese herb extracted from Bolbostemma paniculatum (Maxim.), induces apoptosis in a number of human cancer cell lines. TBMS1 has been reported to induce apoptosis in human glioma cells, however the mechanism remains to be elucidated. The present study explored TBMS1‑induced PI3K/Akt‑related pathways in human glioma cells. The human glioma U251 and the human astrocyte (HA) cell lines were treated with various concentrations of TBMS1. MTT assays were conducted to analyze cell viability. Cell cycle distribution and the rate of apoptosis were assessed using flow cytometry. BrdU incorporation and Hoechst 33342 staining were performed to analyze the cell cycle and apoptosis, respectively. Western blotting was performed to investigate protein expression levels. The results demonstrated that TBMS1 reduced cell viability in human glioma cells U251 by suppressing Akt phosphorylation. Subsequently, TBMS1 inhibited DNA synthesis and induced G2/M phase arrest by targeting the PI3K/Akt/p21 and the cyclin‑dependent kinase 1/cyclin B1 signaling cascades. In addition, TBMS1 triggered apoptosis via the PI3K/Akt‑mediated Bcl‑2 signaling pathway. These results demonstrated that TBMS1 prevented the progression of gliomas via the PI3K/Akt‑dependent pathway, which provided a theoretical basis for in vivo studies to use TBMS1 as potential therapy for the prevention of cancer.
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