Table 2.
Properties | References |
---|---|
Physiological substrates: Prostaglandins (PG) ( H1, H2, H3, G2), 15-keto-prostaglandin H2, 6-keto-prostaglandin F1α, 15-hydroperoxyeicosatetraenoic acid, 10-hydroperoxyoctadeca-8,12-dienoic acid | (Hecker and Ullrich 1989; Ullrich and Hecker 1990; Yeh et al. 2005; Chiang et al. 2006; Yeh et al. 2007; Cathcart et al. 2010; Nakayama 2010; Pan et al. 2016) |
Function: Prostacyclin synthase, isomerization of prostaglandin H2 to prostacyclin (PGI2) (Fig. 3), inhibition of platelet activation and aggregation and induction of vasodilation. Believed to have anti-tumor effects as overexpression has been shown to be chemopreventive in a murine model of the disease, suggesting that the expression and activity of this enzyme may protect against tumor development. |
|
Inhibition: Risk of essential hypertension, myocardial infarction and cerebral infarction (Chiang et al. 2006) | |
Inhibitors: | |
Drugs: | |
Actinomycin D a (Camacho et al. 2008) | |
Cycloheximide a (Camacho et al. 2008) | |
Cyclosporine a (Sharanek et al. 2015) | |
Miconazole, clotrimazole b (Yeh et al. 2005) | |
Minoxidil b (Yeh et al. 2005; Li et al. 2008) | |
Rofecoxib c (Griffoni et al. 2007) | |
Simvastatin a (Skogastierna et al. 2013) | |
Tranylcipromine b (Ding et al. 2002) | |
Other compounds: | |
Imidazole derivatives (4-phenylimidazole, 1-phenylimidazole, 1-benzylimidazole) b (Yeh et al. 2005) | |
U46619, U51605, or U44069 (PGH2 analogues) b (Wada et al. 2004; Yeh et al. 2005; Li et al. 2008; Chao et al. 2011) | |
Induction: Enhanced activity in tumor cells, potential anti-neoplastic and chemopreventive activity | |
Inducers: | |
Natural compounds: | |
13-cis-Retinoic acid, 9-cis-retinoic acid, all-trans- retinoic acid d (Camacho et al. 2008) | |
13-cis-Retinoic acid, 9-cis-retinoic acid, all-trans- retinoic acid d (Camacho et al. 2008) | |
Curcumin d (Tan et al. 2011) | |
Grape seed procyanidin extract d (Mao et al. 2016) | |
13-cis-Retinoic acid, 9-cis-retinoic acid, all-trans- retinoic acid d (Camacho et al. 2008) | |
Physiological compounds: | |
17β-Estradiol d (Korita et al. 2004) | |
Physiological condition: | |
Hypoxia e (Camacho et al. 2011; Wang et al. 2013) | |
Pregnancy d (Okahara et al. 1998) | |
Shear stress e (Korita et al. 2002) |
Footnotes:
Reduced/suppressed mRNA and/or protein level/expression and activity
Competitive inhibition, ligand binding
Decreased/suppressed/inhibited activity/product formation
Up-regulation of biosynthesis, increased expression of protein
Increased transcription/mRNA/protein expression/levels /and/or catalytic activity