Table 1.
In vitro effects of ginger and its constituents against various GI cancer models.
| Cancer | Effects | Reference |
|---|---|---|
| Liver | ||
| HepG2 | Induce apoptosis by activation of caspase-3 | [13] |
| Liver microsomes | Inhibit CYP450, 1-aminobenzotriazole, and aldo-keto reductase Prevent the formation of M14 and M15 and 18β-glycyrrhetinic acid |
[14] |
| SMMC-7721 | Inhibit the phosphorylation of eIF2α and triggered apoptosis | [15] |
| HeoG2 | Release cathepsin D and subsequently cytochrome c Induce apoptosis and intracellular ROS generation and reduced glutathione |
[16] |
| PC12 | Inhibit xanthine oxidase and H2O2-induced damage | [17] |
| HepG2/Hep3B | Decrease the MMP-9 activity and increase the TIMP-1 expression Decrease urokinase-type plasminogen activator activity in Hep3B cells |
[18] |
| Hep-2 | Dose-dependently suppress cell proliferation | [19] |
| Mahlavu cells | Activate caspases 3/7 resulting in the DNA fragmentation | [20] |
| RL34 | Activate the Nrf2/ARE-dependent detoxification pathway | [21] |
| Pancreas | ||
| PaCa | Inhibit mRNA expression and protein secretion of angiogenic factors and NF-κB activity | [22] |
| PANC-1, BxPC | Downregulate of NF-κB signaling and cell survival regulators including COX-2, cyclin D1, survivin, cIAP-1, XIAP, Bcl-2, and MMP-9 and sensitize to gemcitabine | [23] |
| β-cell (INS-1E) | Induce Ca2+ signals in the β-cell by activating the TRPV1 channels | [24] |
| PANC-1 | Decrease invasion and metastasis and NF-κB translocation via downregulation of the ERK pathway | [25] |
| PANC-1 | Upregulate p53, p21 proteins level and ROS production | [26] |
| HPAC, BxPC-3 | Decrease cyclin A, Cdk, Rb phosphorylation, and p53 expression | [27] |
| Gastric Cancer | ||
| HUVE-AGS | Inhibit cell proliferation, VEGF expression, and NF-κB activity | [28] |
| kBZ Jurkat | inhibit COX-2 activation and reduce H. pylori-induced inflammation | [29] |
| HGC/AGS/and KATO III | Inhibit TRAIL-induced NF-κB activation, cIAP1 expression Increase TRAIL-induced caspase-3/7 activation |
[30] |
| JB6 | Inhibit the growth of all Helicobacter pylori strains | [31] |
| Colorectal | ||
| Caco-2 | Inhibit cytochrome P450 enzymes (CYP1A2 and CYP2C8) | [32] |
| HCT116 | Act as antiproliferative agents and enhance the chemotherapeutic effect of 5-FU | [33] |
| COLO 205 | Induce apoptosis, cytochrome c release, caspase activation, and DNA fragmentation Upregulate the Bax, Fas, and FasL and downregulate Bcl-2 and Bcl-XL proteins |
[34] |
| HCT116 | Suppress cyclin D1 expression and induced NAG-1 expression Inhibit beta-catenin, PKC-epsilon, and GSK-3 beta pathways |
[35] |
| HCT116 | Potentiate TRAIL-induced apoptosis and upregulate of TRAIL death receptors (DR-4/-5) Inhibit extracellular signal-regulated kinase 1/2 and p38-MAPK |
[36] |
| Cholangiocarcinoma | ||
| CCA (CL-6) | Upregulate MDR1 and MRP3 genes | [37] |
| KIM-1 | Induce programmed cell death through endonuclease activation and induction of p53 | [38] |
| KMC-1 | caspase 3 activation, potentiate free-radical formation and accumulation of sphinganine |
CYP450, cytochrome P450; eIF2α, eukaryotic initiation factor 2 alpha; ROS, reactive oxygen species; TIMP-1, tissue inhibitor of metalloproteinase 1; Nrf2, nuclear factor (erythroid-derived 2)-like 2; ARE, antioxidant response element; COX-2, cyclooxygenase-2; cIAP-1, cellular inhibitor of apoptosis protein-1; XIAP, X-linked inhibitor of apoptosis protein; MMP-9, matrix metallopeptidase-9; NF-κB, nuclear factor kappaB; ERKs, extracellular-signal-regulated kinase; Rb, retinoblastoma; VEGF, vascular endothelial growth factor; TRAIL, TNF-related apoptosis-inducing ligand; NAG-1, nonsteroidal anti-inflammatory drug- (NSAID-) activated gene-1; PKC, protein kinase C; GSK-3 beta, glycogen synthase kinase-3 beta; MDR1, multidrug resistance gene-1; MRP3; multidrug resistance protein 3.