title: Capsaicin, a spicy component of hot pepper, induces apoptosis by activation of the peroxisome proliferator-activated receptor gamma in HT-29 human colon cancer cells.
abstract: Capsaicin (N-vanillyl-8-methyl-alpha-nonenamide), a spicy component of hot pepper, is a homovanillic acid derivative that preferentially induces certain cancer cells to undergo apoptosis and has a putative role in cancer chemoprevention. Peroxisome proliferator-activated receptor gamma(PPARgamma), a member of the nuclear receptor superfamily, is a ligand-dependent transcription factor. PAPRgamma activation results in growth arrest and/or apoptosis in a variety of cancer cells. In the present study, we investigated the potential of capsaicin to induce apoptotic cell death in human colon cancer cells and the association of PPARgamma in the capsaicin action. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. PPARgamma and vanilloid receptor type 1 (VR-1) expressions at the protein or mRNA levels were detected by western blot analysis and reverse transcription-polymerase chain reaction. Apoptotic cell death was determined by DNA fragmentation and quantified by enzyme-linked immunosorbent assay. HT-29 human colon cancer cells expressed PPARgamma and VR-1. Treatment with capsaicin or the PPARgamma ligand troglitazone induced apoptotic cell death in a dose-dependent manner in HT-29 human colon cancer cells. Capsaicin-induced cell death was completely blocked by bisphenol A diglycidyl ether, a specific PPARgamma antagonist. Capsazepine, a specific antagonist for vanilloid receptor, did not inhibit capsaicin-induced apoptosis. Our data suggest that capsaicin-induced apoptotic cell death in HT-29 human colon cancer cells could be associated with the PPARgamma pathway without the involvement of the vanilloid receptor. Capsaicin may have a beneficial effect for the treatment of colon cancer.
authors.affiliation: Department of Food Science and Nutrition, University of Ulsan, Ulsan.
authors.forename: Chu-Sook
authors.initials: CS
authors.lastname: Kim
authors.forename: Won-Hyung
authors.initials: WH
authors.lastname: Park
authors.forename: Jun-Young
authors.initials: JY
authors.lastname: Park
authors.forename: Ji-Hye
authors.initials: JH
authors.lastname: Kang
authors.forename: Mi-Ock
authors.initials: MO
authors.lastname: Kim
authors.forename: Teruo
authors.initials: T
authors.lastname: Kawada
authors.forename: Hoon
authors.initials: H
authors.lastname: Yoo
authors.forename: In-Seob
authors.initials: IS
authors.lastname: Han
authors.forename: Rina
authors.initials: R
authors.lastname: Yu
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D001559:Benzhydryl Compounds; D002211:Capsaicin / Q000031:analogs & derivatives* / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D003110:Colonic Neoplasms / Q000188:drug therapy; D053938:DNA Fragmentation; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D019073:HT29 Cells; D006801:Humans; D047495:PPAR gamma / Q000037:antagonists & inhibitors / Q000187:drug effects* / Q000378:metabolism; D010636:Phenols / Q000494:pharmacology; D011955:Receptors, Drug / Q000378:metabolism; D050916:TRPV Cation Channels; D000098826:Bisphenol A Compounds
chemical_list: D000970:Antineoplastic Agents; D001559:Benzhydryl Compounds; D002211:Capsaicin; D047495:PPAR gamma; D010636:Phenols; D011955:Receptors, Drug; D050916:TRPV Cation Channels; C494484:TRPV1 receptor; C071423:capsazepine; C006780:bisphenol A; D000098826:Bisphenol A Compounds