ArticleMolecular biology reports2010
beta-Ionone-induced apoptosis in human osteosarcoma (U2os) cells occurs via a p53-dependent signaling pathway.
Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 23 citations in OpenAlex.
- New perspective: Symbiotic pattern and assembly mechanism ofFrontiers in microbiology · 2023Article
- The potential chemotherapeutic effect of β-ionone and/or sorafenib against hepatocellular carcinoma via its antioxidant effect, PPAR-γ, FOXO-1, Ki-67, Bax, and Bcl-2 signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Caudatin induces cell cycle arrest and caspase-dependent apoptosis in HepG2 cell.Molecular biology reports · 2012Article
- PNAS-4 expression and its relationship to p53 in colorectal cancer.Molecular biology reports · 2012Article
- DLC-1 as a modulator of proliferation, apoptosis and migration in Burkitt's lymphoma cells.Molecular biology reports · 2011Article
- SDF-1α inhibits hypoxia and serum deprivation-induced apoptosis in mesenchymal stem cells through PI3K/Akt and ERK1/2 signaling pathways.Molecular biology reports · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
beta-Ionone is a constituent of vegetables and fruits, and can induce apoptosis in some types of malignant cells. However, the mechanism of apoptosis in osteosarcoma (U2os) cells is currently unclear. In this study, we determined whether beta-ionone can induce apoptosis in U2os cells in vitro and which signal pathway(s) is involved. We found that beta-ionone inhibited cell proliferation in U2os cells in a concentration- and time-dependent manner and caused cell cycle arrest at the G1-S phase. TUNEL assay, DNA ladder and assessment of Caspase 3 activity showed that apoptosis was the determinant in the effects of beta-ionone. Furthermore, Expression of the p53 protein increased in a concentration-dependent and time-dependent manner according to immunocytochemistry and immunoblotting after beta-ionone treatment. In addition, beta-ionone upregulated Bax protein and downregulated Bcl2 protein which led to Bax translocation and cytochrome c release, subsequently activated Caspase 3, thus resulting in apoptosis. In summary, these data suggested that beta-ionone induced apoptosis in a concentration-dependent manner in U2os cells via a p53-dependent mitochondrial pathway.
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