AKR1C3, is an enzyme which belongs to the aldo/keto reductase family. It is expressed in many tissues including adrenal gland, brain, kidney, liver, lung, mammary gland, placenta, small intestine, colon, spleen, prostate and testis. AKR1C3 catalyzes the conversion of aldehydes and ketones to alcohols. It catalyzes the reduction of prostaglandin (PG) D2, PGH2 and phenanthrenequinone (PQ) and the oxidation of 9-alpha,11-beta-PGF2 to PGD2,which functions as a bi-directional 3-alpha-, 17-beta- and 20-alpha HSD. It can interconvert active androgens, estrogens and progestins with their cognate inactive metabolites.
Aldo-Keto Reductase 1C4/AKR1C4 is a member of the aldo/keto reductase family that consists of more than 40 known enzymes and proteins. AKR1C4 has highly expressed in Liver. It can catalyzes the bioreduction of chlordecone, a toxic organochlorine pesticide, to chlordecone alcohol in liver. AKR1C4 catalyzes the transformation of the potent androgen dihydrotestosterone (DHT) into the less active form, 5-α-Androstan-3-α,17-β-diol (3-α-diol). In addition, AKR1C4 also has some 20-α-Hydroxysteroid Dehydrogenase activity.
v-akt murine thymoma viral oncogene homolog 1 (AKT1), or protein kinase B-alpha (PKB-ALPHA) is a serine-threonine protein kinase, belonging to the Protein Kinase Superfamily. AKT1 is a major mediator of the responses to insulin, insulin-like growth factor 1 (IGF1), and glucose. AKT1 also plays a key role in the regulation of both muscle cell hypertrophy and atrophy. AKT1 activity is required for physiologic cardiac growth in response to IGF1 stimulation or exercise training. In contrast, AKT1 activity was found to antagonize pathologic cardiac growth that occurs in response to endothelin 1 stimulation or pressure overload. AKT1 selectively promotes physiological cardiac growth while AKT2 selectively promotes insulin-stimulated cardiac glucose metabolism. AKT1 deletion prevented tumor initiation as well as tumor progression, coincident with decreased Akt signaling in tumor tissues. AKT1 is the primary Akt isoform activated by mutant K-ras in lung tumors, and that AKT3 may oppose AKT1 in lung tumorigenesis and lung tumor progression. A number of separate studies have implicated AKT1 as an inhibitor of breast epithelial cell motility and invasion. AKT1 may have a dual role in tumorigenesis, acting not only pro-oncogenically by suppressing apoptosis but also anti-oncogenically by suppressing invasion and metastasis.
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