Antitumor Activity of Capsaicin on Human Colon Cancer Cells in Vitro and Colo 205 Tumor Xenografts in Vivo

Department of Clinical Pathology, Cheng Hsin General Hospital, Taipei 112, Taiwan.
Journal of Agricultural and Food Chemistry (Impact Factor: 3.11). 11/2010; 58(24):12999-3005. DOI: 10.1021/jf103335w
Source: PubMed

ABSTRACT Capsaicin was reported to inhibit cancer cell growth. The aim of this study was to evaluate the antitumor potential of capsaicin by studying antitumor activity in vitro as well as in vivo. The in vitro studies are to examine the effects of capsaicin on human colon cancer colo 205 cells after exposure to capsaicin. The results showed that capsaicin induced cytotoxic effects in a time- and dose-dependent manner and increased reactive oxygen species (ROS) and Ca(2+) but decreased the level of mitochondrial membrane potential (ΔΨ(m)) in colo 205 cells. Data from Western blotting analysis indicated that the levels of Fas, cytochrome c, and caspases were increased, leading to cell apoptosis. Capsaicin decreased the levels of anti-apoptotic proteins such as Bcl-2 and increased the levels of pro-apoptotic proteins such as Bax. Capsaicin-induced apoptosis in colo 205 cells was also done through the activations of caspase-8, -9 and -3. In vivo studies in immunodeficient nu/nu mice bearing colo 205 tumor xenografts showed that capsaicin effectively inhibited tumor growth. The potent in vitro and in vivo antitumor activities of capsaicin suggest that capsaicin might be developed for the treatment of human colon cancer.

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    • "More recently, anticancer activity of capsaicin has been demonstrated [6]. Capsaicin-mediated apoptosis and/or antiproliferative potential has been reported for numerous cancer cell lines, e.g., in leukemia cells [7], multiple myeloma cells [8], cutaneous cell carcinoma [9], glioma cells [10], tongue cancer cells [11], nasopharyngeal carcinoma cells [12], esophageal carcinoma cells [13], gastric cancer cells [14], pancreatic cancer cells [15], hepatocarcinoma cells [16], colon carcinoma cells [17], small cell lung cancer [18], breast cancer cells [19] and prostate cancer cells [20]. It is widely accepted that capsaicin-associated anticancer effects may be executed by reactive oxygen species (ROS) production, cell cycle arrest, regulation of transcription factor expression and changes in growth/survival signal transduction pathways, such as EGFR/HER-2 pathway or NF-␬B inactivation [9,15,19,21–24]. "
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    ABSTRACT: Capsaicin is the major pungent component of the hot chili peppers of the genus Capsicum, which are consumed worldwide as a food additive. More recently, the selective action of capsaicin against cancer cells has been reported. Capsaicin was found to induce apoptosis and inhibit proliferation of a wide range of cancer cells in vitro, whereas being inactive against normal cells. As data on capsaicin-induced genotoxicity are limited and the effects of capsaicin against human lung A549 and DU145 prostate cancer cells were not explored in detail, we were interested in determining whether capsaicin-associated genotoxicity may also provoke A549 and DU145 cell death. Capsaicin-induced decrease in metabolic activity and cell proliferation, and changes in the cell cycle were limited to high concentrations used (≥100μM), whereas, at lower concentrations, capsaicin stimulated both DNA double strand breaks and micronuclei production. Capsaicin was unable to provoke apoptotic cell death when used up to 250μM concentrations. Capsaicin induced oxidative stress, but was ineffective in provoking the dissipation of the mitochondrial inner transmembrane potential. A different magnitude of p53 binding protein 1 (53BP1) recruitment contributed to diverse capsaicin-induced genotoxic effects in DU145 and A549 cells. Capsaicin was also found to be a DNA hypermethylating agent in A549 cells. In summary, we have shown that genotoxic effects of capsaicin may contribute to limited susceptibility of DU145 and A549 cancer cells to apoptosis in vitro, which may question the usefulness of capsaicin-based anticancer therapy, at least in a case of lung and prostate cancer. Copyright © 2015 Elsevier B.V. All rights reserved.
    Mutation Research/Genetic Toxicology and Environmental Mutagenesis 02/2015; 779:23-34. DOI:10.1016/j.mrgentox.2015.02.003 · 2.48 Impact Factor
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    • "Therefore, the relationship between intracellular ROS levels and apoptosis of cancer cells may be dependent upon the differentiated phenotype of cancer cell, and despite the numerous studies in this area, the roles which the regulation of ROS play in the initiation and progression of cancer and the induction of apoptosis are not well understood. NF-B is a ubiquitous and evolutionarily conserved transcription factor that regulates the expression of genes involved in the transformation, survival, proliferation, invasion, angiogenesis, metastasis, and drug resistance of tumor cells (Gupta et al. 2010; Luqman and Pezzuto 2010). Constitutively, active NF- B has now been identified in tissues from most cancer patients. "
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    ABSTRACT: Human exposure to capsaicin, the most abundant pungent chili pepper component, is ubiquitous. Evaluation of capsaicin's carcinogenic potential has produced variable results in in vitro and in vivo genotoxicity and carcinogenicity assays. The capsaicin tested in older studies was often from pepper plant extracts and included other capsaicinoids and diverse impurities. Recent studies utilizing high-purity capsaicin and standardized protocols provide evidence that the genotoxic and carcinogenic potential of capsaicin is quite low and that the purity of capsaicin is important. Several small epidemiological studies suggest a link between capsaicin consumption and stomach or gall bladder cancer, but contamination of capsaicin-containing foods with known carcinogens renders their interpretation problematic. The postulated ability of capsaicin metabolites to damage DNA and promote carcinogenesis remains unsupported. Anticancer activities of capsaicin have been widely reported, as it inhibits the activity of carcinogens and induces apoptosis in numerous cancer cell lines in vitro and explanted into rodents. Diverse mechanisms have been postulated for capsaicin's anticancer properties. One hypothesis is that inhibition of cytochrome P450 enzymes-particularly CYP2E1-retards carcinogen activation but is contradicted by the low potency of capsaicin for CYP inhibition. The potential for dietary capsaicin to act as a chemopreventative is now widely postulated.
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