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. 2021 May 19;12(14):4307–4321. doi: 10.7150/jca.54637

Figure 3.

Figure 3

Representation of metabolism of cholesterol epoxides. 5,6α-EC and 5,6β-EC are metabolites produced by oxidation of cholesterol, then specifically 5,6α-EC is hydrated by Cholesterol epoxide hydrolase (ChEH), originating cholestan-3β,5α,6β-triol (CT). ChEH is a heterodimeric complex integrated by 3β-hydroxysteroid-∆8-∆7-isomerase (D8D7I) and 3β-hydroxysteroid-∆7-reductase (DHCR7). Later, CT is metabolized into 6-oxo-cholestan-3β, 5α-diol (OCDO) by 11-β-hydroxysteroid dehydrogenase of type 2 (11HSD2), OCDO is a promoter of cancer cell proliferation. OCDO is an agonist of the glucocorticoid receptor (GR) and it is translocated to the nucleus. Glucocorticoid induces the expression of genes associated with protection against cell apoptosis. Dendrogenin A (DDA) pathway is represented, which is synthesized from 5,6α-EC and histamine (His); DDA could induce autophagy in cancer cells. Adapted from: 147, 155, 157.