Differential expression of type 2 3α/type 5 17β-hydroxysteroid dehydrogenase (AKR1C3) in tumors of the central nervous system

International Journal of Clinical and Experimental Pathology

Qing Yang¹  Aubrey L Park¹  Hsueh-Kung Lin¹  Naina L Gross¹  Craig H Rabb¹  Chor Wing Sing¹  Timothy B Mapstone¹  Michael D Martin¹  Kar-Ming Fung¹  Michael Fan¹  Mary K Gumerlock¹ 

关键词: AKR;    aldo-keto reductase;    AR;    androgen receptor;    ER;    estrogen receptor;    HSD;    hydroxysteroid dehydrogenase;    PG;    prostaglandin;    PR;    progesterone receptor;    PPAR;    peroxisome proliferator activating receptor;   

DOI  :  

学科分类：生理学与病理学

来源: e-Century Publishing Corporation

【 摘 要 】

Human aldo-keto reductase (AKR) 1C3, type 2 3α-hydroxysteroid dehydrogenase (HSC)/ type 5 17β-HSD, is known to be involved in steroids, prostaglandins, and lipid aldehydes metabolism. The expression of AKR1C3 has been demonstrated in hormone-dependent normal tissues such as breast, endometrium, prostate, and testis; and de -regulated AKR1C3 expression has been shown in breast carcinoma, endometrial hyperplasia, endometrial carcinoma, and prostate carcinoma. AKR1C3 expression has also been demonstrated in hormone-independent normal tissues (renal tubules and urothelium) and neoplastic tissues (renal cell carcinoma, Wilm's tumor, and urothelial cell carcinoma). Extensive expression of AKR1C3 in normal and neoplastic as well as hormone-dependent and hormone-independent tissues indicates that AKR1C3 may have functions beyond steroid hormone metabolism. In this report, we describe a widespread expression of AKR1C3 in glial neoplasms and meningiomas, with limited expression in medulloblastoma and no expression in Schwannoma. These tumors, except meningioma, are not classically considered to be sex hormone-dependent or related brain tumors. The current results corroborate our earlier observations that AKR1C3 is expressed in both sex hormone-dependent and hormone-independent malignancies. Similar to AKR1C3 distribution in Wilm’s tumor, we also demonstrate that expression of AKR1C3 is reduced in tumors with embryonic phenotypes.

【 授权许可】

Unknown