ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2013
Zebularine-induced apoptosis in Calu-6 lung cancer cells is influenced by ROS and GSH level changes.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Zebularine Boosts Imatinib Efficacy in Cells of Colorectal Cancer via Wnt-Survivin-P-Glycoprotein Pathway.Journal of biochemical and molecular toxicology · 2026Article
- Implications of reactive oxygen species in lung cancer and exploiting it for therapeutic interventions.Medical oncology (Northwood, London, England) · 2022Review
- Epigenetics of lung cancer: a translational perspective.Cellular oncology (Dordrecht, Netherlands) · 2019Review
- DNMT3a promotes proliferation by activating the STAT3 signaling pathway and depressing apoptosis in pancreatic cancer.Cancer management and research · 2019Article
- The DNA methyltransferase inhibitor zebularine exerts antitumor effects and reveals BATF2 as a poor prognostic marker for childhood medulloblastoma.Investigational new drugs · 2017Article
- The pro-oxidant buthionine sulfoximine (BSO) reduces tumor growth of implanted Lewis lung carcinoma in mice associated with increased protein carbonyl, tubulin abundance, and aminopeptidase activity.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Capilliposide Isolated from Lysimachia capillipes Hemsl. Induces ROS Generation, Cell Cycle Arrest, and Apoptosis in Human Nonsmall Cell Lung Cancer Cell Lines.Evidence-based complementary and alternative medicine : eCAM · 2014Article
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2 authors at 1 institution in 1 country.
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Abstract
Zebularine (Zeb) is a DNA methyltransferase (DNMT) inhibitor that has various biological properties including anti-cancer effect. In the present study, we evaluated the effects of Zeb on the growth and death of Calu-6 lung cancer cells in relation to reactive oxygen species (ROS) and glutathione (GSH) levels. Zeb inhibited the growth of Calu-6 cells with an IC50 of approximately 150 μM at 72 h in a dose-dependent manner. Zeb induced an S phase arrest of the cell cycle and apoptosis in Calu-6 cells. Pan-caspase inhibitor (Z-VAD) and caspase-8 inhibitor (Z-IETD) significantly rescued some cells from Zeb-induced Calu-6 cell death. In relation to ROS and GSH levels, O2 (•-) level was significantly increased in Zeb-treated Calu-6 cells and caspase inhibitors reduced O2 (•-) level in these cells. Zeb induced GSH depletion in HeLa cells, which was attenuated by caspase inhibitors. L-buthionine sulfoximine (BSO), a GSH synthesis inhibitor, intensified the apoptotic cell death, ROS level, and GSH depletion in Zeb-treated Calu-6 cells. In addition, BSO increased Bax protein and decreased Bcl-2 protein in Zeb-treated Calu-6 cells. In conclusion, Zeb inhibited the growth of Calu-6 lung cancer cells via cell cycle arrest and caspase-dependent apoptosis and its cell death was influenced by ROS and GSH level changes.
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