Table 1. Effects of tocopherol treatment in experimental cancer models.
Type of Cancer | Treatment | Experimental Model | Effects | Ref |
---|---|---|---|---|
Prostate Cancer | γ-T | TRAP rats | ↓Adenocarcinoma | [44] |
↑Apoptosis | ||||
γ-TmT | TRAMP mice | ↓Tumor incidence, PIN | [45] | |
↑Nrf2, HMOX1, GPx, SOD | ||||
γ-TmT | TRAMP mice | ↓Tumor incidence, Nrf2 methylation | [47] | |
↑Nrf2 | ||||
γ-TmT | LNCaP cells | ↑Apoptosis | [48] | |
LNCaP xenograft | ↓Tumor growth | |||
δ-T | LNCaP, VCaP cells | ↓AR activity, PSA | [49] | |
↑Apoptosis | ||||
LNCaP xenograft | ↓Tumor growth | |||
γ-T | LNCaP xenograft | ↓Tumor growth | [52] | |
γ-T + MSA | 22Rv1 xenograft | ↓Tumor growth, Ki67 | [53] | |
↑Bax, Bad, apoptosis | ||||
γ-T | PC-3 cells | ↓Cell growth | [54] | |
↑PPARγ, 15-S-HETE | ||||
α-TOS | PC-3 cells | ↓Autophagy | [55] | |
α-TOS+VK3+ascorbate | PC-3 xenograft | ↓Tumor growth | ||
α-T, γ-T | LNCaP, PC-3 cells | ↓p-Akt | [57] | |
↑PHLPP1 | ||||
| ||||
Breast Cancer | γ-TmT | NMU-treated rats | ↓Tumor growth, p-Akt, ERα | [56] |
↑PPARγ | ||||
δ-T, γ-T | NMU-treated rats | ↓Tumor growth, p-Akt, ERα | [9] | |
↑PPARγ, Nrf2, p21, p27, c-caspase-3 | ||||
γ-TmT | ACI rat early hyperplasia | ↓8-oxo-dG, 8-isoprostane, nitrotyrosine | [58] | |
↑Nrf2, GPx, catalase, SOD | ||||
γ-TmT | ACI rat hyperplasia | ↓8-isoprostane, PGE2, COX2, ERα | [59] | |
↑Nrf2, PPARγ | ||||
γ-TmT | ACI rats | ↓Tumor growth, PCNA | [8] | |
↑CYP1A1, Nrf2, PPARγ | ||||
α-TEA + trastuzumab | MDA-MB-453 xenograft | ↑Tumor regression, apoptosis | [60] | |
α-TEA + MEK/mTOR inhibitors | MCF-7, HCC-1954 cells | ↓p-Akt, p-Erk, p-mTOR, IRS-1 | [61] | |
↑Apoptosis | ||||
α-TEA | MCF-7, HCC-1954 cells | ↓c-FLIP | [62] | |
↑TRAIL, DR5, apoptosis | ||||
Mito-ChM | 9 breast cancer cell lines | ↓Cell growth | [63] | |
MDA-MB-231 xenograft | ↓Tumor growth | |||
TGPS | MCF-7, MDA-MB-231cells | ↓p-Akt, Bcl2 | [65] | |
↑G1/S arrest, apoptosis | ||||
ESeroS-GS | MDA-MB-231 cells | ↓Cell growth, migration, invasion | [66] | |
| ||||
Colon Cancer | γ-TmT | AOM + DSS-treated mice | ↓Inflammation, adenocarcinoma | [7] |
γ-T | AOM + DSS-treated mice | ↓Inflammation, tumor multiplicity | [67] | |
α-TOA | DMH-treated rats | ↓Aberrant crypt foci, COX2 | [68] | |
γ-T, δ-T, TP, TQ | HCT116, HT29 cells | ↓Cell growth, colony formation | [69] | |
↑Apoptosis | ||||
γ-T + lovastatin | HT29 cells | ↑c-caspase-3, apoptosis | [70] | |
| ||||
Lung Cancer | γ-TmT | CL-13 tumors A/J mice | ↓Tumor growth | [71] |
γ-TmT | NNK + B[a]P-treated mice | ↓Tumor multiplicity, tumor growth | [72] | |
H1299 xenograft | ↓Tumor growth | |||
γ-T, δ-T | H1299 xenograft | ↓Tumor growth, 8-oxo-dG, γ-H2AX | [73] | |
↑c-caspase-3 | ||||
| ||||
Other Cancers | ||||
Gastric | α-TOS | SGC-7901 cells | ↓NFκB, Bcl2 family proteins | [74] |
↑c-caspase-3, 9 | ||||
Leukemia | α-TOS | APL mice | ↓Leukemia, MRC complex I | [75] |
↑ROS, caspases, apoptosis | ||||
Esophageal | Vitamin E + selenium | NMBA-treated rats | ↓Tumor growth, NFκB, proliferation | [76] |
Skin | α-T + vitamin C + ferulic acid | UVB-treated SKH-1 mice | ↓Tumor growth, tumor multiplicity | [77] |
Abbreviations: γ-TmT, a natural tocopherol mixture rich in γ-T; T, tocopherol; MSA, methaneseleninic acid; α-TOS, α-tocopheryl succinate; VK3, vitamin K3; α-TEA, α-tocopheryl acetic acid; Mito-ChM, Mito-chromanol; TRAP, transgenic rat for adenocarcinoma of prostate; TRAMP, the transgenic adenocarcinoma of the mouse prostate; NMU, N-methyl-N-nitrosourea; ACI, August Copenhagen Irish; AOM, azoxymethane; DSS, dextran sulfate sodium; DMH, 1,2-dimethylhydrazine; NNK, 4-(methylnitrosoamino)-1-(3-pyridyl)-1-butanone; B[a]P, benzo[a]pyrene; TGPS, D-alpha-tocopheryl polyethylene glycol succinate; ESeroSGS, γ-L-glutamyl-S-[2-[[[3,4- dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1-benzopyran-6-yl]oxy] carbonyl]-3-[[2-(1H-indol-3-yl) ethyl] amino]-3-oxopropyl]-L-cysteinylglycine sodium salt; TP, tocopherol phosphates; TQ, tocopherol quinones; NMBA, N-nitrosomethylbenzylamine.