TABLE 1
Phenolic compounds and in vivo derivatives included in the study and the main reported properties related to antitumor potential.
| Compound | Chemical Structure | CAS Number | Biologic Activities |
|---|---|---|---|
| Uro-A |  | 1143-70-0 | Decreases clonogenic efficiency and cell proliferation through cell cycle arrest in the G(0)/G(1) and G(2)/M stages, followed by induction of apoptosis in HT-29 cells (Kasimsetty et al., 2010) |
| Inhibits Wnt signaling in the human 293T cell line (Sharma et al., 2010) | |||
| Decreases inflammatory markers, including iNOS, COX-2, prostaglandin E synthase, and PGE2, in colonic mucosa (Larrosa et al., 2010b) | |||
| Inhibits aromatase activity in live cell assay (Adams et al., 2010) | |||
| Inhibits cell proliferation and reduces oxidative stress status in bladder cancer (Qiu et al., 2013) | |||
| Uro-B |  | 1139-83-9 | Decreases clonogenic efficiency and cell proliferation through cell cycle arrest in the G(0)/G(1) and G(2)/M stages, followed by induction of apoptosis in HT-29 cells (Kasimsetty et al., 2010) |
| Inhibits aromatase activity in live cell assay (Adams et al., 2010) | |||
| Inhibits cell proliferation and reduces oxidative stress status in bladder cancer (Qiu et al., 2013) | |||
| Resveratrol |  | 501-36-0 | In combination with quercetin, decreases the generation of ROS and increases the antioxidant capacity in HT-29 colon cancer cells (Del Follo-Martinez et al., 2013) |
| Exhibits anticancer activity through caspase-3 cleavage and PARP cleavage induction in HT-29 colon cancer cells (Del Follo-Martinez et al., 2013) | |||
| Inhibits cell proliferation in HCT116 and Caco2 colon cancer cells (Fouad et al., 2013) | |||
| Dihydrocaffeic acid |  | 1078-61-1 | Reduces the cytotoxicity and proinflammatory cytokine production (IL-6 and IL-8) in human keratinocyte cell line HaCaT (Poquet et al., 2008) |
| Homovanillic acid and derivatives |  | 306-08-1 | Induces apoptosis in leukemic cells through oxidative stress (Ito et al., 2004) |
| Gallic acid |  | 149-91-7 | Decreases Caco-2 cell viability through cell cycle arrest at G(0)/G(1), caspase-3 activation, DNA fragmentation, and nuclear condensation (Forester et al., 2014) |
| Inhibits transcription factors NF-κB, AP-1, STAT-1, and OCT-1, which are known to be activated in CRC (Forester et al., 2014) | |||
| Protects against DNA oxidation by activation of antioxidant enzymes (superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase-π) and a decrease of intracellular ROS concentrations in lymphocytes (Ferk et al., 2011) | |||
| Exhibits antioxidant and anticarcinogenic activity against 1,2-dimethyl hydrazine–induced rat colon carcinogenesis (Giftson et al., 2010) | |||
| 3-O-Methylgallic acid |  | 3934-84-7 | Decreases Caco-2 cell viability through cell cycle arrest at G(0)/G(1), caspase-3 activation, DNA fragmentation, and nuclear condensation (Forester et al., 2014) |
| Inhibits transcription factors NF-κB, AP-1, STAT-1, and OCT-1, which are known to be activated in CRC (Forester et al., 2014) | |||
| 4-O-Methylgallic acid |  | 4319-02-2 | Inhibits VEGF production under hypoxic conditions, as well as production of ROS in the endothelial cells stimulated with VEGF (Jeon et al., 2005) |
| Inhibits endothelial cell invasion and tube formation stimulated with bFGF (Jeon et al., 2005) | |||
| Inhibits the expression and production of inflammatory genes and mediators such as NO, PGE2 (as well as the expression of iNOS, COX-2, and TNF-α), and IL-1β in mouse leukemic monocyte macrophage cell line RAW264.7 and in primary macrophages stimulated with LPS (Na et al., 2006) | |||
| EA |  | 476-66-4 | Prevents rat colon carcinogenesis induced by 1,2-dimethylhydrazine through inhibition of the AKT/phosphoinositide-3 kinase pathway (Umesalma and Sudhandiran, 2011) |
| Exhibits anti-inflammatory property by iNOS, COX-2, TNF-α, and IL-6 downregulation due to inhibition of NF-κB and exerts its chemopreventive effect on colon carcinogenesis (Umesalma and Sudhandiran, 2010) | |||
| Induces apoptosis via mitochondrial pathways in colon cancer Caco-2 cells but not in normal colon cells (Larrosa et al., 2006) | |||
| Induces downregulation of the mitogenic IGF-II, activates p21 (waf1/Cip1), mediates a cumulative effect on the G1/S transition phase, and causes apoptotic cell death in SW480 colon cancer cells (Narayanan and Re, 2001) | |||
| Inhibits Wnt signaling in a human 293T cell line (Sharma et al., 2010) | |||
| Inhibits cell proliferation and reduces oxidative stress status in bladder cancer (Qiu et al., 2013) | |||
| Reduces cancer cell viability by apoptosis induction associated with decreased ATP production in Caco-2, MCF-7, Hs 578T, and DU 145 cancer cells without any toxic effect on the viability of normal human lung fibroblast cells (Losso et al., 2004) | |||
| Exhibits anti-PLA2 activity, an enzyme that stimulates the growth of the human pancreatic cancer cell line, and correlates with HER2 overexpression and mediates estrogen-dependent breast cancer cell growth (Da Silva et al., 2008) | |||
| Exhibits antimutagenic activity in Salmonella typhimurium (Smart et al., 1986) | |||
| 3,3′-DiOMEA |  | 2239-88-5 | Exhibits anti-PLA2 activity, an enzyme that stimulates the growth of the human pancreatic cancer cell line, and correlates with HER2 overexpression and mediates estrogen-dependent breast cancer cell growth (Da Silva et al., 2008) |
| Exhibits antimutagenic activity in S. typhimurium (Smart et al., 1986) | |||
| 4,4′-DiOMEA |  | 3374-77-4 | Exhibits antimutagenic activity in S. typhimurium (Smart et al., 1986) |
bFGF, basic fibroblast growth factor; CAS, Chemical Abstracts Service; IL, interleukin; iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide; NF-κB, nuclear factor κ-light-chain-enhancer of activated B cells; NO, nitric oxide; PARP, ADP ribose polymerase; ROS, reactive oxygen species; TNF-α, tumor necrosis factor-α; VEGF, vascular endothelial cell growth factor.