Table 1.

Effect of dietary agents on CaP

Dietary agentIn vitro studiesIn vivo studiesEpidemiologic studies/clinical trials
SeleniumDecrease 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 EModulation 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 DPromotes 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)
LycopeneInduction 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 teaInhibition 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)
PomegranateAntiinvasive, 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)
SilymarinInduction 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)
ResveratrolInduction 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-carbinolInhibition 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)
PhytoestrogensInduction 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)