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Overexpression of a key regulator of lipid homeostasis, Scap, promotes respiration in prostate cancer cells
Author(s) -
Prabhu Anika Vinayak,
Krycer James Robert,
Brown Andrew John
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.02.040
Subject(s) - lncap , regulator , sterol regulatory element binding protein , respiration , prostate cancer , cholesterol , prostate , endocrinology , sterol , carcinogenesis , medicine , chemistry , biology , microbiology and biotechnology , biochemistry , cancer research , cancer , gene , anatomy
Prostate metabolism is unique, characterised by cholesterol accumulation and reduced respiration. Are these related? We modulated cholesterol levels and despite changes in mitochondrial cholesterol content, we saw no effects on lactate production or respiration. Instead, these features may be related via sterol regulatory element‐binding protein 2 (SREBP‐2), the master transcriptional regulator of cholesterol synthesis. SREBP‐2 diverts acetyl‐CoA into cholesterol synthesis and may thus reduce respiration. We examined LNCaP cells overexpressing the SREBP‐2 regulator, Scap: although having higher SREBP‐2 activity, these cells displayed higher respiration. This striking observation warrants further investigation. Given that SREBP‐2 and Scap are regulated by factors driving prostate growth, exploring this observation further could shed light on prostate carcinogenesis.