Table 4.
Other studies that show the effect of N. sativa on cancer cell lines
| Cancer cell line (s) | Roles of apoptosis | Reference |
|---|---|---|
| Human renal adenocarcinoma and normal renal epithelial | Bcl2 is under-expressed, P53 is over-expressed, and caspases 3, 8, and 9 are activated. | 94 |
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| ||
| Human colon cancer cells (Caco-2, HCT-116, LoVo, DLD-1 and HT-29) | Apoptosis was induced via the generation of ROS. TQ increased the phosphorylation states of the MAPK, JNK and ERK. | 117 |
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| ||
| Fibrosarcoma (HT1080) | NSO produced a concentration-dependent inhibition of t-PA, u-PA and PAI-1. | 118 |
| Plasminogen activation system (modulation of the fibrinolytic potential of fibrosarcoma) is depleted. | ||
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| ||
| Squamous cell carcinoma (SCC VII) and fibrosarcoma (FsaR) | RNA expression of p53 and the downstream p53 target gene inhibition of anti-apoptotic Bcdl-2 is increased several fold. | 119 |
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| ||
| HL-60 cells | Apoptosis is induced by activating caspase-3 and 8. | 120 |
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| ||
| PC3 | Cell proliferation is inhibited by TQ, and the activations of AKT and extracellular signal-regulated kinase are suppressed. Vascular endothelial growth factor–induced extracellular signal-regulated kinase activation is inhibited. | 121 |
| Acts as an angiogenesis inhibitor. | ||
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| ||
| Human multiple myeloma cells | Both constitutive and IL-6-inducible STAT3 phosphorylation, which correlated with the inhibitions of c-Src and JAK2 activations, are inhibited. Signal transducer and activator of the transcription 3 activation pathway is suppressed. | 122 |
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| ||
| Human lung cancer cell line | Cell viability is reduced and the cellular morphology of A-549 cells is altered in a concentration-dependent manner. | 123 |
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| Osteosarcoma (SaOS-2) | TQ significantly blocked human umbilical vein endothelial cell tube formation in a dose-dependent manner. | 124 |
| TQ significantly downregulated NF-κB DNA-binding activity, XIAP, survivin and VEGF. | ||
| Expressions of cleaved caspase-3 and Smac were upregulated in SaOS-2 cells. | ||
| NF-κB and its regulated molecules and anti-angiogenesis effects are suppressed. | ||
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| ||
| Primary effusion lymphoma (PEL) cell lines | Constitutive activation of AKT via generation of ROS is downregulated and conformational changes in Bax protein, leading to the loss of mitochondrial membrane potential and the release of cytochrome c to the cytosol, are caused. | 125 |
| Caspase-9, caspase-3, and polyadenosine 5′-diphosphate ribose polymerase cleavage are activated, leading to caspase-dependent apoptosis. | ||
| TQ is a potent inducer of apoptosis in PEL cells via release of ROS. | ||
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| ||
| Hepatic stellate cells | TQsignificantly attenuated the expression of CD14 and Toll-like receptor 4. | 126 |
| TQ also significantly inhibited phosphatidylinositol 3-kinase andserine/threonine kinase-protein kinase B phosphorylation. | ||
| Expressions of α-SMA and collagen-I were significantly decreased by TQ. | ||
| TQ decreased XIAP and cellular FLIP expression, which are related with the regulation of apoptosis. | ||
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| Mouse neuroblastoma (Neuro-2a) cells | Bax/Bcl-2 ratio is increased. | 127 |
| Caspase-3 is activated, along with downregulation of XIAP. | ||
AKT, protein kinase B; ERK, extracellular signal-regulated kinase; JNK, janus kinase; MAPK, mitogen- activated protein kinases; PAI-1, plasminogen activator inhibitor type 1; ROS, reactive oxygen species; STAT3, signal transducer and activator of transcription 3; t-PA, tissue-type plasminogen activator; u-PA, urokinase-type plasminogen activator; VEGF, vascular endothelial growth factor; XIAP, X-linked inhibitor of apoptosis protein.