ArticleThe Journal of international medical research2019
Paris polyphylla 26 triggers G2/M phase arrest and induces apoptosis in HepG2 cells via inhibition of the Akt signaling pathway.
Article in The Journal of international medical research, 2019. 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.
- Bioassay-Guided Procedure Coupled with HR-ESIMS Dereplication for Isolation of Antiproliferative Bromo-Tyramine Derivative fromMarine drugs · 2025Article
- Research progress of Paris polyphylla in the treatment of digestive tract cancers.Discover oncology · 2024Review
- Evaluation of the effect of GSK-3β on liver cancer based on the PI3K/AKT pathway.Frontiers in cell and developmental biology · 2024Review
- In Vitro Cytotoxic Effect of Aqueous Extracts from Leaves and Rhizomes of the SeagrassBiology · 2023Article
- Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesParis polyphylla 26 (PP-26) is a monomer purified from Paris polyphylla, which has traditionally been used as an antimicrobial, hemostatic, and anticancer agent in China. The anti-proliferation effect and underlying molecular mechanism of PP-26 were investigated in vitro.
methodsThe effects of PP-26 on various tumor cells were detected by MTT assay. PP-26-affected cell cycle and cell cycle-related proteins in HepG2 cells were detected by flow cytometry and western blotting, respectively. Apoptosis in response to PP-26 was assessed by Hoechst 33258 staining and flow cytometry. PP-26-affected apoptosis-related proteins and Akt signaling were detected by western blotting. The inhibitory effect of PP-26 on HepG2 cells, when combined with 5-fluorouracil (5-FU), was also assessed.
resultsPP-26 inhibited proliferation of HepG2 cells in a dose-dependent manner by triggering G2/M-phase arrest. Moreover, PP-26 induced apoptosis of HepG2 cells. Expression levels of apoptosis proteins caspase 9, caspase 3, PARP, Bcl-2, Bcl-xL, and Mcl-1 were downregulated, while the expression level of apoptosis protein Bax was upregulated. Expression levels of p-Akt, p-GSK-3β, and p-Foxo3 were downregulated. Combination with PP-26 enhanced 5-FU inhibition of HepG2 cell proliferation.
conclusionsPP-26 triggers G2/M-phase arrest and induces apoptosis in HepG2 cells via inhibition of the Akt signaling pathway.
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