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Fenretinide: A p53-independent way to kill cancer cells

Lookup NU author(s): Professor Penny Lovat, Dr Chris Redfern

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Abstract

The synthetic retinoid fenretinide [N-(4 hydroxyphenyl)retinamide] induces apoptosis of cancer cells and acts synergistically with chemotherapeutic drugs, thus providing opportunities for novel approaches to cancer therapy. The upstream signaling events induced by fenretinide include an increase in intracellular levels of ceramide, which is subsequently metabolized to GD3. This ganglioside triggers the activation of 12-Lox (12-lipoxygenase) leading to oxidative stress and apoptosis via the induction of the transcription factor Gadd153 and the Bcl-2-family member protein Bak. Increased evidence suggests that the apoptotic pathway activated by fenretinide is p53-independent and this may represent a novel way to treat tumors resistant to DNA-damaging chemotherapeutic agents. Therefore, fenretinide offers increased clinical benefit as a novel agent for cancer therapy, able to complement the action of existing chemotherapeutic treatment regimes. Furthermore, synergy between fenretinide and chemotherapeutic drugs may facilitate the use of chemotherapeutic drugs at lower concentrations, with possible reduction in treatment-associated morbidity. © 2005 Elsevier Inc. All rights reserved.


Publication metadata

Author(s): Corazzari, M., Lovat, P.E., Oliverio, S., Di Sano, F., Donnorso, R., Redfern, C.P.F., Piacentini, M.

Publication type: Review

Publication status: Published

Journal: Biochemical and Biophysical Research Communications

Year: 2005

Volume: 331

Issue: 3

Pages: 810-815

Print publication date: 10/06/2005

ISSN (print): 0006-291X

ISSN (electronic): 1090-2104

URL: http://dx.doi.org/10.1016/j.bbrc.2005.03.184

DOI: 10.1016/j.bbrc.2005.03.184

PubMed id: 15865936


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