Capsaicin binds to prohibitin 2 and displaces it from the mitochondria to the nucleus
- Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama (Japan)
- Department of Integrative Medical Biology, School of Medicine, Keio University, Tokyo (Japan)
- Department of Hematology, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama (Japan)
Capsaicin is widely used as a food additive and as an analgesic agent. Besides its well-known role in nociception, which is mediated by vanilloid receptor 1 specifically expressed in dorsal root ganglion neurons, capsaicin has also been considered as a potential anticancer agent, as it inhibits cell proliferation and induces apoptosis in various types of cancer cells. Here we identified a new molecular target of capsaicin from human myeloid leukemia cells. We show that capsaicin binds to prohibitin (PHB) 2, which is normally localized to the inner mitochondrial membrane, and induces its translocation to the nucleus. PHB2 is implicated in the maintenance of mitochondrial morphology and the control of apoptosis. We also provide evidence suggesting that capsaicin causes apoptosis directly through the mitochondria and that PHB2 contributes to capsaicin-induced apoptosis at multiple levels. This work will serve as an important foundation for further understanding of anticancer activity of capsaicin.
- OSTI ID:
- 21255871
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 379, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2008.12.103; PII: S0006-291X(08)02510-2; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
Similar Records
RPF101, a new capsaicin-like analogue, disrupts the microtubule network accompanied by arrest in the G2/M phase, inducing apoptosis and mitotic catastrophe in the MCF-7 breast cancer cells
Induction apoptosis of luteolin in human hepatoma HepG2 cells involving mitochondria translocation of Bax/Bak and activation of JNK