Premium
Altered retinoid metabolism in breast cancer
Author(s) -
Pingitore Attilio,
Perri Mariarita,
Cione Erika,
Kane Maureen A.
Publication year - 2011
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.25.1_supplement.lb324
Subject(s) - retinoid , retinoic acid , retinol , cell growth , cancer cell , retinoid x receptor , cancer research , apoptosis , cancer , breast cancer , vitamin , endocrinology , biology , chemistry , programmed cell death , medicine , microbiology and biotechnology , nuclear receptor , biochemistry , gene , transcription factor
Cancer, a disease of uncontrolled cell growth arising from aberrant cell proliferation, differentiation and apoptosis is the second leading cause of death in the United States with 26% of new cases attributed to breast cancer. The term “retinoids” describes compounds that include vitamin A (retinol), its metabolites, and synthetic analogs that exhibit vitamin A activity. Retinoic Acid (RA) is an active metabolite of vitamin A and is essential to a wide range of physiological processes, including cell proliferation, cell differentiation, and apoptosis. RA homeostasis is maintained through dietary intake of retinol, and its storage, mobilization, transport, and biosynthesis into RA. The biosynthesis and shuttling of RA to specific nuclear receptors (RAR, RXR, and/or PPARb/d) dictates the outcome of RA signaling. Defective RA metabolism in local populations of cells is thought to be a main initiator of mammary tumor formation and progression. With robust and rigorous analytical methods (LC‐MS/MS) we have studied retinol metabolism in a panel of breast cancer cells together with biochemical and genetic insights into the mechanisms involved in the disruption of vitamin A metabolism in mammary carcinoma.