期刊
BRITISH JOURNAL OF PHARMACOLOGY
卷 178, 期 16, 页码 3248-3260出版社
WILEY
DOI: 10.1111/bph.15205
关键词
breast; cancer treatment; cholesterol; metabolic switch; oncometabolism; oxysterol; targeted therapy
资金
- Institut Claudius Regaud
- Institut National du Cancer [PRTK 2016-O36, PLBIO-2018-145, PRTK-2015-118]
- Ligue Nationale Contre le Cancer [labellisation 2019]
- Fondation Toulouse Cancer Sante [2017CS065, 2019CS093]
- Association pour la Recherche sur le Cancer [PJA 2013 12 00 342]
- Fondation de France [R11166BB]
- Epoxcan
Metabolic pathways play critical roles in cancer development, with cholesterol metabolism pathway in breast cancer offering potential therapeutic targets. Inhibiting oncosterone metabolism could be a novel approach for breast cancer treatment, while activating cell re-differentiation and chemoprevention show promising prospects for therapy.
Metabolic pathways have emerged as cornerstones in carcinogenic deregulation providing new therapeutic strategies for cancer management. Recently, a new branch of cholesterol metabolism has been discovered involving the biochemical transformation of 5,6-epoxycholesterols (5,6-ECs). The 5,6-ECs are metabolized in breast cancers to the tumour promoter oncosterone whereas, in normal breast tissue, they are metabolized to the tumour suppressor metabolite, dendrogenin A (DDA). Blocking the mitogenic and invasive potential of oncosterone will present new opportunities for breast cancer treatment. The reactivation of DDA biosynthesis, or its use as a drug, represents promising therapeutic approaches such as DDA-deficiency complementation, activation of breast cancer cell re-differentiation and breast cancer chemoprevention. This review presents current knowledge of the 5,6-EC metabolic pathway in breast cancer, focusing on the 5,6-EC metabolic enzymes ChEH and HSD11B2 and on 5,6-EC metabolite targets, the oxysterol receptor (LXR beta) and the glucocorticoid receptor.
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