Effect of dietary agents on CaP
| Dietary agent | In vitro studies | In vivo studies | Epidemiologic studies/clinical trials |
|---|---|---|---|
| Selenium | Decrease in AR and PSA, increase in TRAIL-mediated apoptosis (8), p53 phosphorylation, induction of Bax, loss of mitochondrial membrane potential, cytochrome c release, activation of caspase-9 and caspase-3 (94), inhibition of mitogen-activated protein kinase, PI3K pathways (10) | Inhibition of CaP development, increase in p27, decrease in proliferating cell nuclear antigen, AR expression, serum PSA levels (9) | Decrease in CaP incidence (16, 17) |
| Vitamin E | Modulation of transforming growth factor-β, AR/PSA signaling (21), DNA synthesis arrest induction of apoptosis, decrease in vascular endothelial growth factor and inhibition of matrix metalloproteinases (22) | Disruption of PI3K/Akt pathway, regulation of phosphoinositide homeostasis, tumor growth inhibition (26, 27), decrease in CaP incidence, decrease in PSA, increase in median survival time, induction of apoptosis (95, 96) | Decrease in CaP incidence α-tocopherol β-carotene trial (29), SU.VIMAX trial (30) |
| No significant association between vitamin E levels and CaP risk (31, 32) | |||
| Vitamin D | Promotes differentiation, inhibits proliferation, invasion and metastasis, decrease in cyclooxygenase-2, increase in PGDH (34, 35) | Decrease in CaP growth and tumors, reduction in PIN (44) | Decrease in CaP incidence, decrease in PSA (36-39, 44) |
| Lycopene | Induction of apoptosis, inhibits cell proliferation, metastatis and cell invasion, decrease in cyclin D1, cell cycle G0-G1 arrest (46, 47) | Prevents oxidative DNA damage (45), inhibits CaP growth and decrease in PSA, IGF-I, IL-6, and 5α-reductase (48), induction of phase II enzymes like GPx, glutathione S-transferase, GR and glutathione, 8-oxodGuo levels, prevention of lipid damage (49) | Decrease in CaP incidence and PSA levels (50-53) |
| No significant association between lycopene levels and CaP risk (54-56) | |||
| Green tea | Inhibition of cell growth, induction of apoptosis, induction of p21, p53, and Bax (57), inhibition of HIF-1α degradation, inhibition of PSA-triggered basement membrane degradation, and matrix metalloproteinase-2 activation (97, 98), inhibition of 5α-reductase (60) and ODC activity (61) | Overexpression of clusterin (59), decrease in IGF-I and increase in IGF-binding protein-3 levels in TRAMP, inhibition of tumor growth and PSA secretion (62), decrease CaP progression with reduction of S100A4 and restoration of E-cadherin (63) | Decreased CaP risk (64, 67) |
| Minimal activity against CaP (65, 66) | |||
| Pomegranate | Antiinvasive, antiproliferative, antimetastatic effects (69) | Reduction in tumor growth and decrease in serum PSA levels (68) | Prolongation of PSA doubling time (70) |
| Induction of apoptosis, increase in Bax, Bak, p21/p27, decrease in cyclins D1, D2, and E, cdk2, cdk4, cdk6, Bcl-xL, and Bcl2 (68) | |||
| Silymarin | Induction of cell cycle arrest, Increases cdks, cyclins, p21, p27, modulates epidermal growth factor receptor, IGF-I, NF-κB pathways (72), inhibition of telomerase and decrease in PSA inhibition of AR, with down-regulation of prostate epithelium-derived Ets transcription factor, human glandular kallikrein, and FKBP51(73, 74) | Decrease in CaP growth, down-regulation of proliferating cell nuclear antigen, cyclin D1, vascular endothelial growth factor, and CD31 (72) | Delay in PSA progression (75) |
| Resveratrol | Induction of apoptosis and cell cycle arrest, increase in p53 (76) modulation of HSP27 and HSP70 (78), TRAIL-induced apoptosis with survivin depletion (79), modulates Src-Stat3 signaling, inhibits protein kinase C–mediated Erk1/Erk2 activation (80), inhibits NF-κB activation, down-regulates PSA, AR, ARA24 (76) | ||
| Indole-3-carbinol | Inhibition of cell growth, induction of apoptosis, down-regulation of Bcl-2, Bcl-xL, survivin, IAP, XIAP, c-FLIP, increase in Bax, release of cytochrome c and caspase activation, down-regulation of cyclins D1 and E, CDK2, CDK4, CDK6, up-regulation of p15, p21, p27, p53, modulation of PI3K/Akt, mitogen-activated protein kinase, NF-κB pathways, inhibition of SP1, ER, AR, Nrf2 (82), augments TRAIL-mediated apoptosis (83), induces BRCA1 and BRCA2 genes (84) | Decrease in CaP growth and metastases (85) | |
| Phytoestrogens | Induction of apoptosis, inhibition of angiogenesis (86), modulates 5α-reductase, tyrosine kinase, topoisomerase, P450 aromatase (87), inhibition of cell growth, decreases PSA levels (88) down-regulates PART-1 gene (92) | Reduction in tumor growth with decrease in serum PSA levels (88, 89) | Decreased CaP risk (90) |