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Capsaicin induces apoptosis in human small cell lung cancer via the TRPV pathway
Author(s) -
Crabtree Clayton M.,
Dom Aaron M.,
Lau Jamie K.,
Brown Kathleen C.,
Shiflett Brandon S.,
Witte Theodore R.,
Hardman W. Elaine,
Dasgupta Piyali
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.143.4
Subject(s) - capsaicin , apoptosis , trpv1 , pharmacology , cancer research , chemistry , human lung , cell , trpv , inflammation , medicine , receptor , lung , biochemistry , transient receptor potential channel
Capsaicin, the spicy ingredient of chili peppers, is used to topically treat pain and inflammation associated with a variety of diseases. However, emerging evidence shows that it can induce apoptosis in different transformed cell types in vitro and in animal models. The present study examines the apoptotic activity of capsaicin in human small cell lung cancer (SCLC). Here we show that capsaicin induced apoptosis in a panel of human SCLC in a concentration‐dependent and time‐dependent manner. Most importantly, capsaicin caused 5–6 fold apoptosis in a panel of human SCLC cell lines, but did not affect normal human lung epithelial cells. The dietary administration of capsaicin decreased the growth of H69 and DMS53 human SCLC tumors xenotransplanted in nude mice. The apoptotic activity of capsaicin was independent of TRPV1, the known receptor for capsaicin. In contrast, depletion of TRPV6 by siRNA ablated the apoptotic activity of capsaicin. Our findings suggest that capsaicin may have potential applications as a novel agent for management and therapy of human SCLCs.