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Literature summary extracted from

  • Mantel, A.; Carpenter-Mendini, A.; VanBuskirk, J.; Pentland, A.P.
    Aldo-keto reductase 1C3 is overexpressed in skin squamous cell carcinoma (SCC) and affects SCC growth via prostaglandin metabolism (2014), Exp. Dermatol., 23, 573-578.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

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

Protein Variants

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

Natural Substrates/ Products (Substrates)

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
-
?

Organism

EC Number Organism UniProt Comment Textmining
1.1.1.188 Homo sapiens P42330
-
-

Source Tissue

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
-

Substrates and Products (Substrate)

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
-
?

Synonyms

EC Number Synonyms Comment Organism
1.1.1.188 AKR1C3
-
Homo sapiens
1.1.1.188 aldo-keto reductase 1C3
-
Homo sapiens

Cofactor

EC Number Cofactor Comment Organism Structure
1.1.1.188 NADP+
-
Homo sapiens

Expression

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

General Information

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