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Cancer | Effect | Mechanism | Concentration | Reference |
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Many human cancer cell lines | Cell death | Cu(I)- or Fe(II)-dependent H2O2 formation, oxidative stress | P | 6-10 |
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CRC with KRAS or BRAF mutations, human cell lines, and mouse xenografts | Cell death | Inactivation of GAPDH, depletion of glutathione, ROS increase, decreased ATP, energetic crisis | P | 75 |
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AML human cell line | Apoptosis, inhibition of proliferation | ERK phosphorylation, Raf1/MAPK inhibition | P/D(?) | 57 |
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Breast or colon human cell line | Cell death | Changes in metabolomic profile, NAD deficiency | P | 79 |
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Gastric cancer patients, cell lines | Inhibition of proliferation | Selective upregulation of TMEFE2 | D | 81 |
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Many cancer cell lines | Killing cancer cells by synergistic or additive action with anticancer drugs, including bleomycin, sorafenib, and auranofin | DNA double-strand break induction; modification of redox balance | P/D | 85-87 |
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All cancers | Killing cancer cells by stimulation of the immune system | Fas-induced apoptosis, reduction of the activity of caspase-3, caspase-8, and caspase-10, reduced ROS levels, and increased permeability of the mitochondrial membrane as well as HIF-1/2 activation in monocytes; NK stimulation by IFN-γ activation | P/D | 3, 93-96 |
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Colorectal cancer | Killing cancer cells by targeting their epigenetic profile | Synergistic or additive effects with DNA-demethylating drugs, TET2 activation | P/D | 103 |
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All cancers | Tumor inhibition by eradication of cancer stem-like cells | Synthetic lethality with targeting glycolysis; TET2 activation; TET1 inhibition; oxidative DNA damage; activation of the MLH1/c-Abl/p73 signaling; inhibition of pluripotency factors, incl. OCT4A, SOX2, and NANOG | P/D(?) | 114-121 |
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All cancers | Metastasis inhibition | Inhibition of MMP secretion; inhibition of hyaluronidase and hyaluronan lyase; increasing efficacy of BET1; upregulation of HDAC1; inhibition epithelial-mesenchymal transition | P/D | 127-137 |
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