ArticleMolecular and cellular biochemistry2010
Induction of apoptosis in hepatocellular carcinoma Smmc-7721 cells by vitamin K(2) is associated with p53 and independent of the intrinsic apoptotic pathway.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Postoperative use of the chemopreventive vitamin K2 analog in patients with hepatocellular carcinoma.PloS one · 2013Pooled it
- Vitamin K (Menaquinone) from marine Kocuria sp. RAM1: optimization, characterization and potential in vitro biological activities.Microbial cell factories · 2025Article
- Vitamin K: Calcium Metabolism Modulator for Menopausal Women.Journal of menopausal medicine · 2024Review
- The biological responses of vitamin K2: A comprehensive review.Food science & nutrition · 2023Review
- Research progress on the anticancer effects of vitamin K2.Oncology letters · 2018Review
- Evaluation of the antitumor effects of vitamin KDrug delivery and translational research · 2018Article
- Clinical Impact of Vitamin K Dosing on Sorafenib Treatment for Hepatocellular Carcinoma.Journal of Cancer · 2017Article
- Vitamin K and hepatocellular carcinoma: The basic and clinic.World journal of clinical cases · 2015Review
- Metabolomics identifies the intersection of phosphoethanolamine with menaquinone-triggered apoptosis in an in vitro model of leukemia.Molecular bioSystems · 2015Article
- Enhanced therapeutic efficacy of vitamin K2 by silencing BCL-2 expression in SMMC-7721 hepatocellular carcinoma cells.Oncology letters · 2012Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitamin K(2) (VK(2)) can exert cell growth inhibitory effects in various human cancer cells. In this study, we investigated the cell growth inhibitory effects of VK(2) in hepatocellular carcinoma Smmc-7721 cells and the mechanisms involved. We found that VK(2)-inhibited cell proliferation in Smmc-7721 cells in a dose-dependent manner, and the IC50 of VK(2) in Smmc-7721 cells was 9.73 microM at 24 h. The data from flow cytometric analyses, DNA fragmentation assays, and caspase 3 activity assays revealed that apoptosis was the determining factor in VK(2) activity. Furthermore, a significant increase in p53 phosphorylation and protein level was exhibited in apoptotic cells treated with VK(2), although there were no changes in p53 mRNA expression. Bax expression was unaffected by VK(2) in Smmc-7721 cells. In addition, our study showed that caspase 3 was activated by caspase 8, not caspase 9, in Smmc-7721 cells treated with VK(2). In summary, these data suggested that VK(2) can inhibit the growth of Smmc-7721 cells by induction of apoptosis involving caspase 8 activation and p53. This apoptotic process was not mediated by the intrinsic apoptotic pathway.
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