RRR‐α‐tocopheryl succinate inhibits the proliferation of human prostatic tumor cells with defective cell cycle/differentiation pathways

Israel, Karen; Sanders, Bob G.; Kline, Kimberly

doi:10.1080/01635589509514404

Cited by 75 publications

(33 citation statements)

References 24 publications

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“…Out of the eight different tocopherols included in the term vitamin E, a-tocopherol often exerts specific functions and is the predominant form of vitamin E found in plasma and tissues, whereas g-tocopherol, and not a-tocopherol, is the major form present in the diet. Besides its antioxidant function, vitamin E and its analogues can modulate transforming growth factor-h and AR/PSA signaling pathway and regulate cell cycle through DNA synthesis arrest in LNCaP, PC-3, and DU-145 CaP cells (21). Induction of apoptosis, by causing depletion of cytosolic Fas with increase in the membrane levels of Fas, decreased production of vascular endothelial growth factor, and inhibition of matrix metalloproteinases are other mechanisms through which vitamin E inhibits prostate carcinogenesis (22).…”

Section: Vitamin Ementioning

confidence: 99%

Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise

Syed

Khan

Afaq

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

164

124

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Prostate cancer (CaP) is second only to lung cancer as the cause of cancer-related deaths in American men and is responsible for over 29,000 deaths per year. One promising approach to reduce the incidence of CaP is through chemoprevention, which has been recognized as a plausible and cost-effective approach to reduce cancer morbidity and mortality by inhibiting precancerous events before the occurrence of clinical disease. Indeed, CaP is an ideal candidate disease for chemoprevention because it is typically diagnosed in the elderly population with a relatively slower rate of growth and progression, and therefore, even a modest delay in the development of cancer, achieved through pharmacologic or nutritional intervention, could result in substantial reduction in the incidence of clinically detectable disease. In this review, we have summarized the recent investigations and mechanistic studies on CaP chemoprevention using dietary agents, such as selenium, vitamins D and E, lycopene, phytoestrogens, flavonoids, and green tea polyphenols. Well-designed trials are required to delineate the potential clinical usefulness of these agents through issues, such as determining the optimal period and route of administration, systemic bioavailability, optimal dosing and toxicity of the agent, and single or combinatorial approach. It is hoped that, combining the knowledge based on agents with targets, effective approaches for CaP chemoprevention can be established. (Cancer Epidemiol Biomarkers Prev 2007;16(11):2193 -203)

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Section: Vitamin Ementioning

confidence: 99%

Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise

Syed

Khan

Afaq

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

164

124

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“…It has been shown to inhibit the growth of several human cancer cell lines including prostate. 6 We have shown that vitamin E induces growth arrest in prostate cancer cell lines mediated by alterations in cell cycle regulatory proteins, particularly p27 Kipl . 7 We have extended our study to determine the interaction between vitamin E and selenium in prostate cancer cell lines.…”

Section: Introductionmentioning

confidence: 99%

Synergistic effect of vitamin E and selenium in human prostate cancer cell lines

Venkateswaran

Fleshner

Klotz

2004

Prostate Cancer Prostatic Dis

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Vitamin E and selenium are the two most popular dietary supplements used to prevent prostate cancer. The hypothesis that these antioxidants reduce prostate risk is being tested in the selenium and vitamin E chemoprevention trial (SELECT). We hypothesize that selenium potentiates vitamin E-induced inhibition of prostate cancer cell growth in vitro. Prostate cancer cell populations growing asynchronously were treated with a combination of vitamin E and selenium and processed for flow cytometric analysis. Prostate cancer cells treated with a combination of the antioxidants revealed that selenium potentiates vitamin Einduced inhibition of LNCaP cells in vitro. This was demonstrated by a reduction in the percentage of cells in the S phase. This crucial finding confirms our previous observations that antioxidant molecules act via distinct mechanistic pathways. These independent biological effects can be exploited in order to augment the anticancer properties of individual agents. These data also validate the two factorial design of the SELECT trial, permitting pairwise comparisons between agents in combination and alone.

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“…Vitamin E succinate (VES) is the succinate derivative of a-tocopherol and has the most effective antitumorigenic activity in a variety of cell culture and animal models (3 -8). The antitumorigenic activity of VES includes inhibition of proliferation (9,10), invasion (11), and angiogenesis (12) and induction of apoptosis (13). VES induces apoptosis in many types of cancer cells, including breast, cervical, endometrial, colon, and prostate.…”

Section: Introductionmentioning

confidence: 99%

Vitamin E succinate induces NAG-1 expression in a p38 kinase-dependent mechanism

Shim

Eling²

2008

Molecular Cancer Therapeutics

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NAG-1 (nonsteroidal anti-inflammatory drug-activated gene), a member of the transforming growth factor-B superfamily, is involved in many cellular processes, such as inflammation, apoptosis/survival, and tumorigenesis. Vitamin E succinate (VES) is the succinate derivative of A-tocopherol and has antitumorigenic activity in a variety of cell culture and animal models. In the current study, the regulation and role of NAG-1 expression in PC-3 human prostate carcinoma cells by VES was examined. VES treatment induced growth arrest and apoptosis as well as an increase in NAG-1 protein and mRNA levels in a time-and concentration-dependent manner. VES treatment induced nuclear translocation and activation of p38 kinase. Pretreatment with p38 kinase inhibitor blocked the VES-induced increase in NAG-1 protein and mRNA levels, whereas an inhibition of protein kinase C, Akt, c-Jun NH 2 -terminal kinase, or MEK activity had no effect on VES-induced NAG-1 levels. Forced expression of constitutively active MKK6, an upstream kinase for p38, induced an increase in NAG-1 promoter activity, whereas p38 kinase inhibitor blocked MKK6-induced increase in NAG-1 promoter activity. VES treatment resulted in >3-fold increase in the half-life of NAG-1 mRNA in a p38 kinase-dependent manner and transient transfection experiment showed that VES stabilizes NAG-1 mRNA through AU-rich elements in 3 ¶-untranslated region of NAG-1 mRNA. The inhibition of NAG-1 expression by small interfering RNA significantly blocked VES-induced poly(ADP-ribose) polymerase cleavage, suggesting that NAG-1 may play an important role in VES-induced apoptosis. These results indicate that VES-induced expression of NAG-1 mRNA/protein is regulated by transcriptional/ post-transcriptional mechanism in a p38 kinase-dependent manner and NAG-1 can be chemopreventive/therapeutic target in prostate cancer. [Mol Cancer Ther 2008; 7(4):961 -71]

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RRR‐α‐tocopheryl succinate inhibits the proliferation of human prostatic tumor cells with defective cell cycle/differentiation pathways

Cited by 75 publications

References 24 publications

Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise

Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise

Synergistic effect of vitamin E and selenium in human prostate cancer cell lines

Vitamin E succinate induces NAG-1 expression in a p38 kinase-dependent mechanism

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