Diet, autophagy, and cancer: A review
ABSTRACT A host of dietary factors can influence various cellular processes and thereby potentially influence overall cancer risk and tumor behavior. In many cases, these factors suppress cancer by stimulating programmed cell death. However, death not only can follow the well-characterized type I apoptotic pathway but also can proceed by nonapoptotic modes such as type II (macroautophagy-related) and type III (necrosis) or combinations thereof. In contrast to apoptosis, the induction of macroautophagy may contribute to either the survival or death of cells in response to a stressor. This review highlights current knowledge and gaps in our understanding of the interactions among bioactive food constituents, autophagy, and cancer. Whereas a variety of food components including vitamin D, selenium, curcumin, resveratrol, and genistein have been shown to stimulate autophagy vacuolization, it is often difficult to determine if this is a protumorigenic or antitumorigenic response. Additional studies are needed to examine dose and duration of exposures and tissue specificity in response to bioactive food components in transgenic and knockout models to resolve the physiologic implications of early changes in the autophagy process.
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ABSTRACT: Wasabia japonica (wasabi) has been shown to exhibit properties of detoxification, anti-inflammation and the induction of apoptosis in cancer cells. This study aimed to investigate the molecular mechanism of the cytotoxicity of wasabi extract (WE) in colon cancer cells to evaluate the potential of wasabi as a functional food for chemoprevention. Colo 205 cells were treated with different doses of WE, and the cytotoxicity was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide. Apoptosis and autophagy were detected by 4',6-diamidino-2-phenylindole, 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl-imidacarbo-yanine iodide and staining for acidic vascular organelles (AVOs), along with Western blotting. The results demonstrated that WE induced the extrinsic pathway and mitochondrial death machinery through the activation of TNF-α, Fas-L, caspases, truncated Bid and cytochrome C. WE also induced autophagy by decreasing the phosphorylation of Akt and mTOR and promoting the expression of microtubule-associated protein 1 light chain 3-II and AVO formation. An in vivo xenograft model verified that tumor growth was delayed by WE treatment. Our studies revealed that WE exhibits anti-colon cancer properties through the induction of apoptosis and autophagy. These results provide support for the application of WE as a chemopreventive functional food and as a prospective treatment of colon cancer.European Journal of Nutrition 02/2015; DOI:10.1007/s00394-015-0866-5 · 3.84 Impact Factor
Article: Vitamin D in cancer chemoprevention[Show abstract] [Hide abstract]
ABSTRACT: There is increasing evidence that Vitamin D (Vit D) and its metabolites, besides their well-known calcium-related functions, may also exert antiproliferative, pro-differentiating, and immune modulatory effects on tumor cells in vitro and may also delay tumor growth in vivo. The aim of this review is to provide fresh insight into the most recent advances on the role of Vit D and its analogues as chemopreventive drugs in cancer therapy. A systematic review of experimental and clinical studies on Vit D and cancer was undertaken by using the major electronic health database including ISI Web of Science, Medline, PubMed, Scopus and Google Scholar. Experimental and clinical observations suggest that Vit D and its analogues may be effective in preventing the malignant transformation and/or the progression of various types of human tumors including breast cancer, prostate cancer, colorectal cancer, and some hematological malignances. These findings suggest the possibility of the clinical use of these molecules as novel potential chemopreventive and anticancer agents.Pharmaceutical Biology 04/2015; DOI:10.3109/13880209.2014.988274 · 1.34 Impact Factor
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ABSTRACT: Autophagy is a complicated self-eating response of cells to external or internal stimuli. This process involves cellular degradation through the lysosomes of dysfunctional or unnecessary cellular components or organelles to maintain basic energy levels. This nonapoptotic programmed cell death, similar to other main phenomena of cell biology such as apoptosis and differentiation, has been implicated in the pathogenesis of a series of disorders, such as neurodegenerative diseases, cardiovascular diseases, and especially in cancer. Increasing evidence has suggested that the autophagy pathways may provide potential targets for cancer intervention, although their precise roles in cancer initiation and progression remain controversial. Natural products are very important sources of chemotherapeutics agents. Regulation of autophagy could be an important mechanism contributing to the beneficial effect of quite a few natural products. Herein, we briefly introduce the characteristics and roles of autophagy in cancer and systematically summarize the natural autophagy regulators, with emphasis on apigenin, berberine, beta-elemene, capsaicin, curcumin, genistein, kaempferol, oridonin, paclitaxel, quercetin, resveratrol, silybin, triptolide, and ursolic acid, with the aim to provide information for novel avenues on cancer therapies based on autophagy.Phytochemistry Reviews 02/2014; 14(1). DOI:10.1007/s11101-014-9339-3 · 2.89 Impact Factor