ArticleDrug design, development and therapy2014
Phyllostachys edulis extract induces apoptosis signaling in osteosarcoma cells, associated with AMPK activation.
Article in Drug design, development and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 13 citations in OpenAlex.
- PHGDH inhibition and FOXO3 modulation drives PUMA-dependent apoptosis in osteosarcoma.Cell death & disease · 2025Article
- Causal effects of metabolites on malignant neoplasm of bone and articular cartilage: a mendelian randomization study.Frontiers in genetics · 2025Article
- Chemical Constituent Profiling ofMolecules (Basel, Switzerland) · 2021Article
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3 authors at 2 institutions in 1 country.
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Abstract
objectiveBamboo is distributed worldwide, and its different parts are used as foods or as a traditional herb. Recently, antitumoral effects of bamboo extracts on several tumors have been increasingly reported; however, antitumoral activity of bamboo extracts on osteosarcoma remains unclear. In the present study, we investigated effects of an aqueous Phyllostachys edulis leaf extract (PEE) on osteosarcoma cells and the underlying mechanism of inhibition.
methodsThe growth of human osteosarcoma cell lines 143 B and MG-63 and lung fibroblast MRC-5 cells was determined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. Apoptosis was demonstrated using TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay and flow cytometric analysis. Phosphorylation and protein levels were determined by immunoblotting.
resultsAfter treatment with PEE, viability of 143 B and MG-63 cells was dose-dependently reduced to 36.3% ± 1.6% of control values, which were similar to AICAR (5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside) treatments. In parallel, ratios of apoptotic cells and cells in the sub-G1 phase were significantly increased. Further investigation showed that PEE treatments led to activation of caspase cascades and changes of apoptotic mediators Bcl2, Bax, and p53. Consistently, our results revealed that PEE activated adenosine monophosphate-activated protein kinase (AMPK) signaling, and the AMPK activation was associated with the induction of apoptotic signaling.
conclusionOur results indicated that PEE suppressed the growth of 143 B and MG-63 cells but moderately affected MRC-5 cells. PEE-induced apoptosis may attribute to AMPK activation and the following activation of apoptotic signaling cascades. These findings revealed that PEE possesses antitumoral activity on human osteosarcoma cells by manipulating AMPK signaling, suggesting that PEE alone or combined with regular antitumor drugs may be beneficial as osteosarcoma treatments.
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