ArticleOncology letters2018
Chrysotoxene induces apoptosis of human hepatoblastoma HepG2 cells
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
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- α-Hederin Increases The Apoptosis Of Cisplatin-Resistant Gastric Cancer Cells By Activating Mitochondrial Pathway In Vivo And Vitro.OncoTargets and therapy · 2019Article
- Nudol, a phenanthrene derivative fromDrug design, development and therapy · 2019Article
- [Role of mitochondrial permeability transition pore in mediating the inhibitory effect of gastrodin on oxidative stress in cardiac myocytesNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have indicated that chrysotoxene may be a potential drug used to treat tumors, however the effect of chrysotoxene on hepatoblastoma remains unknown. Therefore, the present study aimed to investigate the cytotoxic effect and elucidate the potential molecular mechanism of chrysotoxene on human hepatoblastoma HepG2 cells. Chrysotoxene (5-40 µg/ml) exhibited cytotoxic activity against HepG2 cells with inhibitory rates of 24.67-84.06% (half maximal inhibitory concentration, 19.64 µg/ml), observed from a Cell Counting Kit-8 assay. The results of flow cytometry analysis indicated that chrysotoxene (5, 10 or 20 µg/ml) significantly (P<0.01) induced the apoptosis of HepG2 cells with apoptotic rates of 23.14, 35.68 and 55.61% respectively, compared with the control group. The results of western blot analysis indicated that chrysotoxene (5, 10 or 20 µg/ml) significantly (P<0.05) promoted the release of second mitochondria-derived activator of caspase (Smac) and Cytochrome c from the mitochondria to the cytoplasm, downregulated Survivin and B cell lymphoma-2 (Bcl-2) proteins levels, and upregulated Bcl-2-associated X factor (Bax), apoptotic protease activating factor-1 (Apaf-1), cleaved (c)-caspase-9 and c-caspase-3 protein levels in HepG2 cells, compared with the control group. The results of xenograft analysis indicated that chrysotoxene (20 mg/kg) significantly (P<0.01) inhibited the growth of HepG2 cell-induced tumors by regulating the aforementioned apoptotic proteins (Smac, Cytochrome c, Survivin, Bcl-2, Bax, Apaf-1, c-caspase-9 and c-caspase-3), compared with the control group. In conclusion, chrysotoxene induced the apoptosis of HepG2 cells
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