Table 1.
Effect and targets/mechanisms of resveratrol in gastric cancer and colorectal cancer
| Effect | Cell or animal model | Proposed targets/mechanisms | Ref. | |
| Gastric cancer | Anti-H. pylori | MKN-45 cells | Inhibition of IL-8 secretion, inhibition of ROS generation | [27] |
| Mice | Downregulation of IL-8 and iNOS, inhibition of NF-κB activity, activation of the Nrf2/HO-1 pathway | [30] | ||
| Anti-proliferation | KATO-III cells | Inhibition of PKC activity | [34] | |
| ACS cells | The MEK1/2-ERK1/2- c-Jun signaling pathway | [37] | ||
| SNU-1 cells | The PTEN/ PI3K/Akt signaling pathway | [25] | ||
| MGC803 cells | The PI3K/Akt signaling pathway | [38] | ||
| MGC-803 cells | Downregulation of β-catenin, c-myc, and cyclin D1, inhibition of the Wnt/β-catenin pathway | [39] | ||
| Inhibition of invasion and metastasis | SGC7901 cells | Inhibition of the Hh signaling pathway and EMT | [41] | |
| SGC7901 cells | Inhibition of the Raf/MAPK signaling pathway | [44] | ||
| BGC823 cells | Inhibition of MALAT1 | [42] | ||
| Induction of apoptosis and senescence | SGC7901 cells | Downregulation of survivin | [45] | |
| SGC-7901 cells | Increase of ROS | [46] | ||
| AGS, BGC-823 and SGC-7901 cells | Downregulation of the senescence pathways such as cyclin D1, CDK 6 and CDK4, p16 and p21 | [47] | ||
| Nude mice | Downregulation of anti-apoptotic gene bcl-2, up-regulation of the pro-apoptotic gene bax | [52] | ||
| SGC 7901 cells | Upregulation of bax, cleaved caspase 3 and cleaved caspase 8, downregulation of bcl-2, inhibition of NF-κB activity | [53] | ||
| SGC-7901 cells | Activation of caspase-3 and pro-caspase 9 was downregulated, the expression ratio of bax/bcl-2 was increased | [54] | ||
| SNU-1 cells and KATO-III cells | Upregulation of both Fas and Fas-Lin SNU-1 cells, upregulation of Fas-L in KATO-III cells | [56] | ||
| SNU-1, KATO- and RF-1 cells | SNU-1 cells: Upregulation of p53, downregulation of surviving; AGS cells: Upregulation of p53, stimulation of caspase 3 and cytochrome C oxidase activities; KATO-III cells (not expressing p53): Stimulation of caspase 3 and cytochrome C oxidase activities | [57] | ||
| SNU-1 cells | Upregulation of p53 expression | [58] | ||
| MDR | SGC7901/DOX | PTEN/Akt signaling pathway | [62] | |
| RDB and RNOV | In RDB cells, Res reduced the expression level of all analyzed genes, so were results at the protein level obtained for P-gp and TXN. In turn, in the RNOV cell line, Res reduced TXN expression at mRNA and protein levels | [63] | ||
| Colorectal cancer | Anti-inflammatory | HCA-7 cancer cells | Downregulation of COX-2 III | [67] |
| Dextran Sulfate Sodium (DSS) mouse model of colitis | Decrease of CD3+ T cells, downregulation of p53 | [68] | ||
| Caco-2 and SW480 cells | Inhibition of iNOS, decrease of NO production, inhibition of NF-κB activity | [70] | ||
| Mice | Downregulation of Nrf2 | [72] | ||
| Inhibit oxidative stress | Wistar male rats | Increase of the enzymic and non-enzymic antioxidant status | [74] | |
| Anti-proliferation | CaCo-2 cells | Inhibition of ODC expression | [75] | |
| SW480 cells | Modulation of cyclin and CDK activities | [76] | ||
| HT-29 and WiDr cells | Downregulation of telomerase activity | [78] | ||
| HT-29 cells | Inhibition of IGF-1R and the downstream Akt/Wnt signaling pathway | [80] | ||
| HCT116 cells | Downregulation the PTEN/PI3K/Akt and Wnt/β-catenin signaling | [81] | ||
| Induce apoptosis | HCT116 cells | Induction of bax, activation of caspases 3 and 9 | [83] | |
| HT-29 cells | Production of O2 -•, increase of mitochondrial ROS production | [84] | ||
| SW480 cells | Redistribution of Fas | [85] | ||
| HT-29 cells | Lysosomal cathepsin D demonstrated upstream of cytosolic caspase activation | [86] | ||
| HT-29 cells | ROS-triggered autophagy, decrease of cleavage of casapse-8 and caspase-3 | [87] | ||
| HT- 29 cells | The PKC- ERK1/2 signaling pathway | [90] | ||
| Inhibit invasion and metastasis | LoVo and HCT116 cells | Downregulation of MALAT1, decrease of β-catenin attenuation of Wnt/β-catenin signaling | [91] | |
| HCT116 cells | ERK and p38-dependent pathways, downregulation of TCF4 | [93] | ||
| HCT116 and SNU81 colon cancer cells | Increase of TTP expression | [94] | ||
| HCT116 cells | Suppression of NF-κB signaling pathway | [98] | ||
| HCT116, RKO and SW480 cells | Decrease of TNF-β/TNF-βR-induced EMT, suppression of NF-βB and FAK | [99] | ||
| Inhibition of angiogenesis | Caco2 cell and HCT116 cells | Reduction of VEGF level | [105] | |
| Reversion of MDR | 5-FU-sensitive HCT-116 cells | Decrease of the levels of POL-β, POLH, FEN1and DDB2 | [106] | |
| 5-FU chemoresistance-derived clones HCT116R cells | Upregulation of intercellular junctions and downregulation of NF-κB pathway | [107] | ||
| HCT116R cells | Suppression of tumor-promoting factors (NF-κB, MMP-9, CXCR4) activity and EMT factors | [108] | ||
| CIS-resistant HCT 116 cells | Increase in the early apoptosis fraction and enhance the subsequent apoptotic effects of CIS | [109] | ||
| HCT116/LOHP | Downregulation of mRNA and P-gp/MDR1 and MDR1 promoter activity | [110] |
IL: Interleukin; ROS: Reactive oxygen species; NO: Nitric oxide; iNOS: Inducible nitric oxide synthase; Nrf2: Nuclear factor erythroid 2-related factor 2; EMT: Epithelial-mesenchymal transition; Hh: Hedgehog; MALAT1: Metastasis-associated lung adenocarcinoma transcript 1; CIS: Cisplatin; NO: Nitric oxide; MDR1: Multi-drug resistance protein 1.