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Literature summary for 1.1.1.188 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)

Cloned (Comment) Organism
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

Protein Variants Comment Organism
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)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
prostaglandin D2 + NADP+ Homo sapiens
-
9alpha,11beta-prostaglandin F2 + NADPH
-
?

Organism

Organism UniProt Comment Textmining
Homo sapiens P42330
-
-

Source Tissue

Source Tissue Comment Organism Textmining
skin
-
Homo sapiens
-
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)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
prostaglandin D2 + NADP+
-
Homo sapiens 9alpha,11beta-prostaglandin F2 + NADPH
-
?

Synonyms

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

Cofactor

Cofactor Comment Organism Structure
NADP+
-
Homo sapiens

Expression

Organism Comment Expression
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

General Information Comment Organism
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
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