Details

Autor(en) / Beteiligte

• Stevenson, Cathryn
• Crabtree, Clayton
• Dom, Aaron
• Lau, Jamie
• Brown, Kathleen
• Creel, Rebecca
• Damron, C
• Chen, Y
• Witte, Theodore
• Hardman, W
• Dasgupta, Piyali

Titel

Capsaicin causes apoptosis of human small cell lung cancers cells via the TRPV6/calpain pathway (644.8)

Ist Teil von

• The FASEB journal, 2014-04, Vol.28 (S1), p.n/a

Ort / Verlag

The Federation of American Societies for Experimental Biology

Erscheinungsjahr

2014

Link zum Volltext

Quelle

Wiley Online Library - AutoHoldings Journals

Beschreibungen/Notizen

• Small cell lung cancer (SCLC) is characterized by aggressive clinical course and a dismal survival rate. The present study examines the apoptotic activity of capsaicin (the pungent ingredient of chili peppers) in human SCLC. We observed that capsaicin induced apoptosis in a panel of human SCLC in a concentration‐dependent and time‐dependent manner. Most importantly, capsaicin caused robust 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 H69 and DMS53 human SCLC tumors in nude mice and in chicken chorioallantoic membrane (CAM) models. The apoptotic activity of capsaicin was reversed with the generalized TRPV antagonist ruthenium red, indicating that TRPV receptors are involved in capsaicin induced apoptosis. However, antagonists to TRPV1, namely capsazepine and SB‐366791, did not affect the apoptotic activity of capsaicin, suggesting the involvement of a TRPV1‐independent mechanism. In contrast, depletion of TRPV6 by siRNA ablated the apoptotic activity of capsaicin. Capsaicin‐induced apoptosis was also inhibited by calpeptin, a chemical inhibitor of the calpain pathway. Our findings suggest that capsaicin may have potential applications as a novel therapeutic agent for SCLCs. Grant Funding Source: Supported by an NIH R15‐Area Grant, a FAMRI YCSA Grant, and WV INBRE