Journal
NEOPLASMA
Volume 60, Issue 4, Pages 364-372Publisher
VEDA, SLOVAK ACAD SCIENCES
DOI: 10.4149/neo_2013_048
Keywords
colorectal cancer; capsaicin; ROS; EMT; metastasis
Categories
Funding
- Sichuan Province Higher Education Quality Project
- Chengdu Medical College Student Innovation Research and Training Project [CX2010011]
- Scientific Research Fund of Sichuan Provincial Education Department [11ZB207]
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Colorectal cancer (CRC), one of the most common human malignancies, is a major public health problem in the developed world. Capsaicin, widely used as a food additive and as an analgesic agent, is a major pungent ingredient of red pepper. Though capsaicin-induced apoptosis was previously reported in cancer cells, relatively little is known about the impact of capsaicin on other aspect of cancer cell behavior. In this study, we demonstrated that treatment with high-concentration of capsaicin (>= 200 mu M for SW480 and CT-26 cell lines; >= 25 mu M for HCT116 cell line) inhibited CRC cell proliferation in a dose-dependent manner. In spite of no anti-proliferative effect, notably, low-concentration of capsaicin (100 mu M for SW480 and CT-26 cell lines; 12.5 mu M for HCT116 cell line) enhanced both migratory and invasive capability of these cells, which was validated by both in vitro and in vivo model. Further, we showed that 100 mu M capsaicin induced epithelial-to-mesenchymal (EMT), up-regulated expression of MMP-2 and MMP-9, and activated Akt/mTOR and STAT-3 pathways in SW480 cells. Finally, we showed that capsaicin-induced metastasis of CRC cells was mediated by modulating reactive oxygen species (ROS) production. Our findings are considered as a significant step toward a better understanding of capsaicin-associated regulatory network on CRC cells.
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