Capsaicin — A Literature Survey

Monsereenusorn, Yongyot; Kongsamut, Sathapana; Pezalla, Paul D.

doi:10.3109/10408448209003371

Cited by 117 publications

(32 citation statements)

References 88 publications

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“…Capsaicin is the active principle ingredient of the hot chilli pepper Capsicum, which contains about 0.1-1.0% of capsaicin (1). Spicy foods may play some role in human carcinogenesis, and to date one single epidemiological study has demonstrated that there was a correlation between hot chilli pepper consumption and incidence of gastric cancer (2); however, other studies have failed to provide evidence for its genotoxic potential (3,4).…”

Section: Introductionmentioning

confidence: 99%

Induction of Apoptosis in Leukemic Cells by Homovanillic Acid Derivative, Capsaicin, through Oxidative Stress

Ito¹,

Nakazato²,

et al. 2004

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Section: Introductionmentioning

confidence: 99%

Induction of Apoptosis in Leukemic Cells by Homovanillic Acid Derivative, Capsaicin, through Oxidative Stress

Ito¹,

Nakazato²,

et al. 2004

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“…Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide), a vanilloid receptor agonist, is the major pungent principle found in chili peppers of the plant genus Capsicum (Monsereenusorn et al, 1982). This alkaloid compound has an in vitro antiproliferative effect on prostate (Mori et al, 2006;Sa´nchez et al, 2006), colon (Kim et al, 2004), gastric (Lo et al, 2005), hepatic (Jung et al, 2001) and leukemic cancer cells (Ito et al, 2004) while leaving normal cells unharmed (Ito et al, 2004;Athanasiou et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Capsaicin causes cell-cycle arrest and apoptosis in ER-positive and -negative breast cancer cells by modulating the EGFR/HER-2 pathway

et al. 2009

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Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) is an ingredient of chili peppers with inhibitory effects against cancer cells of different origin. We examined the activity of capsaicin on breast cancer cells in vitro and in vivo. The drug potently inhibited growth of ER-positive (MCF-7, T47D, BT-474) and ER-negative (SKBR-3, MDA-MB231) breast cancer cell lines, which was associated with G 0 /G 1 cell-cycle arrest, increased levels of apoptosis and reduced protein expression of human epidermal growth factor receptor (EGFR), HER-2, activated extracellular-regulated kinase (ERK) and cyclin D1. In contrast, cell-cycle regulator p27 KIP1, caspase activity as well as poly-ADP ribose polymerase (PARP) cleavage were increased. Notably, capsaicin blocked breast cancer cell migration in vitro and decreased by 50% the size of MDA-MB231 breast cancer tumors growing orthotopically in immunodeficient mice without noticeable drug side effects. in vivo activation of ERK was clearly decreased, as well as expression of HER-2 and cyclin D1, whereas caspase activity and PARP cleavage products were increased in tumors of drug-treated mice. Besides, capsaicin potently inhibited the development of preneoplastic breast lesions by up to 80% without evidence of toxicity. Our data indicate that capsaicin is a novel modulator of the EGFR/HER-2 pathway in both ERpositive and -negative breast cancer cells with a potential role in the treatment and prevention of human breast cancer.

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“…Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide), a vanilloid receptor agonist, is the principal pungent constituent of the plant genus Capsicum that is present in chilli peppers (1). The relationship of capsaicin to genotoxicity, carcinogenicity, and prevention and treatment of cancer has been widely explored (2).…”

Section: Introductionmentioning

confidence: 99%

Capsaicin induces apoptosis and modulates MAPK signaling in human gastric cancer cells

Park

Kim

Lee

et al. 2013

Molecular Medicine Reports

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Abstract. Capsaicin is known to have tumor suppressive effects. However, the molecular mechanisms and targets of capsaicin involved in exerting anticancer activity are complex and remain to be clarified. The aim of the current study was to investigate the effects of capsaicin on human gastric cancer cells (AGS cells) and demonstrate that capsaicin induced apoptosis in AGS cells. Results of the MTT assay and flow cytometry revealed that capsaicin potentially inhibited the proliferation of AGS cells and induced apoptosis in vitro in a dose-dependent manner. Cleaved caspase-3 was increased and Bcl-2 was reduced by treatment with capsaicin in AGS cells. Capsaicin treatment decreased the expression of phosphorylated ERK 1/2, p38 MAPK or JNK in AGS cells. The results of this study suggest that capsaicin may serve as an anti-tumorigenic agent in human gastric cancer.

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Capsaicin — A Literature Survey

Cited by 117 publications

References 88 publications

Induction of Apoptosis in Leukemic Cells by Homovanillic Acid Derivative, Capsaicin, through Oxidative Stress

Induction of Apoptosis in Leukemic Cells by Homovanillic Acid Derivative, Capsaicin, through Oxidative Stress

Capsaicin causes cell-cycle arrest and apoptosis in ER-positive and -negative breast cancer cells by modulating the EGFR/HER-2 pathway

Capsaicin induces apoptosis and modulates MAPK signaling in human gastric cancer cells

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