EC Number | Cloned (Comment) | Organism |
---|---|---|
1.1.1.188 | SCC cell line is infected with either AKR1C3 overexpressing retroviral construct (SCC-AKR1C3), quantitative AKR1C3 expression analysis in wild-type and mtransfected cells | Homo sapiens |
EC Number | Protein Variants | Comment | Organism |
---|---|---|---|
1.1.1.188 | additional information | AKR1C3 overexpressing skin squamous cell carcinoma, SCC, cells are protected from the antiproliferative effects of prostaglandin D2 | Homo sapiens |
EC Number | Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|---|
1.1.1.188 | prostaglandin D2 + NADP+ | Homo sapiens | - |
9alpha,11beta-prostaglandin F2 + NADPH | - |
? |
EC Number | Organism | UniProt | Comment | Textmining |
---|---|---|---|---|
1.1.1.188 | Homo sapiens | P42330 | - |
- |
EC Number | Source Tissue | Comment | Organism | Textmining |
---|---|---|---|---|
1.1.1.188 | skin | - |
Homo sapiens | - |
1.1.1.188 | squamous cell carcinoma cell | AKR1C3 is overexpressed in skin squamous cell carcinoma (SCC) and affects SCC growth via prostaglandin metabolism | Homo sapiens | - |
EC Number | Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|---|
1.1.1.188 | prostaglandin D2 + NADP+ | - |
Homo sapiens | 9alpha,11beta-prostaglandin F2 + NADPH | - |
? |
EC Number | Synonyms | Comment | Organism |
---|---|---|---|
1.1.1.188 | AKR1C3 | - |
Homo sapiens |
1.1.1.188 | aldo-keto reductase 1C3 | - |
Homo sapiens |
EC Number | Cofactor | Comment | Organism | Structure |
---|---|---|---|---|
1.1.1.188 | NADP+ | - |
Homo sapiens |
EC Number | Organism | Comment | Expression |
---|---|---|---|
1.1.1.188 | Homo sapiens | AKR1C3 is overexpressed in skin squamous cell carcinoma (SCC) and affects SCC growth via prostaglandin metabolism. It is upregulated by its substrate, prostaglandin D2 | up |
EC Number | General Information | Comment | Organism |
---|---|---|---|
1.1.1.188 | malfunction | although attenuating AKR1C3 expression in squamous cell carcinoma cells by siRNA does not affect growth, treatment with PGD2 and its dehydration metabolite, 15delta-PGJ2, decreases squamous cell carcinoma, SCC, proliferation in a PPARgamma-dependent manner. In addition, treatment with the PPARgamma agonist pioglitazone profoundly inhibits squamous cell carcinoma proliferation. SCC-AKR1C3 metabolizes protaglandin D2, PGD2, to 9alpha,11beta-prostaglandin F2 12fold faster than the parent cell line and is protected from the antiproliferative effect mediated by PGD2. PGD2 and its metabolite 15delta-prostaglandin J2 attenuate SCC proliferation in a PPARgamma-dependent manner, therefore activation of PPARgamma by agonists such as pioglitazone may benefit those at high risk of SCC | Homo sapiens |
1.1.1.188 | physiological function | AKR1C3 is overexpressed in skin squamous cell carcinoma (SCC) and affects SCC growth via prostaglandin metabolism. AKR1C3 is overexpressed in various malignancies, suggesting a tumor promoting function. SCC-AKR1C3 metabolizes protaglandin D2, PGD2, to 9alpha,11beta prostaglandin F2. Unlike other AKR1C members, AKR1C3 can synthesize prostaglandin F2alpha from prostaglandin H2, an arachidonic acid derivative synthesized by cyclooxygenase | Homo sapiens |