Vitamin E: A dark horse at the crossroad of cancer management

Abstract

It appears that the story on vitamin E and its role in human health remains incomplete. It is apparent that vitamin E supplementation involves many variables, some of which include its uptake from the intestine, the preference for α-tocopherol, transport by tocopherol specific proteins and lipid transporters and the differential metabolism of different vitamin E isoforms. The fundamental differences within population genetics can have significant implications for the effect that dietary supplementation might have on human health. When evaluating the efficacy of vitamin E prophylactic or therapeutic use in previous and future studies, it is critical to consider dosage to be administered, form of vitamin E and source (such as whether from synthetic or purified from natural sources). Further studies are needed to determine the effects of all vitamin E isoforms on cell growth, tumorigenicity, to clarify its possible use as an adjuvant to existing chemotherapeutics. The Alpha-Tocopherol, Beta Carotene (ATBC) Cancer Prevention Study Group and Selenium and Vitamin E Cancer Prevention Trial (SELECT) studies along with the numerous studies of vitamin E should help guide the next chapter of vitamin E research.

ATP‑binding cassette transporter A1: A promising therapy target for prostate cancer (Review)

“…The efflux of intracellular cholesterol is mediated by reverse cholesterol transporters, such as scavenger receptor class B type I, a membrane receptor with extensive tissue distribution and a number of physiological functions (33). A reduction in Akt-dependent survival signaling may also contribute to the anticancer activity of ABCA1.…”

Vitamin E Transporters in Cancer Therapy

“…TS has shown to be highly selective against different malignant cells, including breast, prostate, lung, stomach, ovary, and colon cancer cells but largely safe to normal cells (17). TS inhibits cancer cell growth by several mechanisms, including (i) inhibition of cell proliferation by blocking G0/G1 cell-cycle mediated in part (17,24,43,47) by mitogen-activated kinases MEK1 and ERK1, and upregulation of the cell cycle regulatory protein p21 (26), (ii) induction of apoptosis that is attributed to TS ability to downregulate the nuclear transcription factor NF-κB (27), and (iii) inhibition of metastasis (28). Findings from the in vitro studies were confirmed in vivo, however only following the intraperitoneal administration of TS which was effective in reducing the incidence of breast, colon, and stomach cancers and melanoma, whereas when given orally TS was ineffective due to extensive hydrolyses by esterases in the gastrointestinal tract (29).…”

“…Clinically, it has been reported that women who developed breast cancer had significantly lower plasma levels of α-tocopherol compared with controls (43). In addition, findings from a large randomized trial conducted to determine if micronutrients could impact the incidence of esophageal, stomach, and overall cancers demonstrated that when grouped with β-carotene and selenium, α-tocopherol had a significant benefit on total mortality when compared with placebo group (43).…”

“…In addition, findings from a large randomized trial conducted to determine if micronutrients could impact the incidence of esophageal, stomach, and overall cancers demonstrated that when grouped with β-carotene and selenium, α-tocopherol had a significant benefit on total mortality when compared with placebo group (43). Also and as part of a randomized, double-blind, placebo-controlled trial called Alpha-Tocopherol, Beta Carotene (ATBC), which investigated the effect of antioxidant supplements on the incidence of lung cancer, male smokers received 50 mg of α-tocopherol daily for 5 to 8 years were found to have significantly reduced incidence of prostate cancer and mortality (44).…”

Bioavailability of Vitamin E

“…cardiovascular diseases and cancers, numerous epidemiological studies have investigated the association between VE dietary intake or status (usually evaluated as the fasting blood -tocopherol concentration) and the incidence of these diseases and reported negative associations (15)(16)(17). However, most randomized controlled trials have failed to show a benefit of VE supplementation on the incidence of these diseases (18,19). Several explanations have been put forward, including an absence of effect of VE supplementation on these diseases (20), a negative effect of -tocopherol supplementation on the bioavailability of other VE isomers (21) or the absence of population stratification by VE status or oxidative stress in these negative studies (19).…”