中枢神经系统肿瘤中2型3α/5型17β-羟基类固醇脱氢酶(AKR1C3)的差异表达。

PubMed ID
发表日期 2010年Mar月

原始出处 国际临床与实验病理学杂志
International journal of clinical and experimental pathology
作者 Park  Aubrey L  Lin  Hsueh-Kung  Yang  Qing  Sing  Chor Wing  Fan  Michael  Mapstone  Timothy B  Gross  Naina L  Gumerlock  Mary K  Martin  Michael D  Rabb  Craig H  Fung  Kar-Ming 

文献标题 中枢神经系统肿瘤中2型3α/5型17β-羟基类固醇脱氢酶(AKR1C3)的差异表达。
Differential expression of type 2 3α/type 5 17β-hydroxysteroid dehydrogenase (AKR1C3) in tumors of the central nervous system.

文献摘要

人醛酮还原酶(AKR)1C3,2型3α-羟基类固醇脱氢酶(HSC)/5型17β-HSD,已知参与类固醇、前列腺素和脂醛代谢。AKR1C3在激素依赖性正常组织如乳腺、子宫内膜、前列腺和睾丸中表达;在乳腺癌、子宫内膜增生、子宫内膜癌和前列腺癌中表达下调。AKR1C3在激素非依赖性正常组织(肾小管和尿路上皮)和肿瘤组织(肾细胞癌、肾母细胞瘤和尿路上皮细胞癌)中也有表达。AKR1C3在正常组织、肿瘤组织、激素依赖性组织和激素非依赖性组织中的广泛表达表明,AKR1C3可能具有类固醇激素代谢以外的功能。在本报告中,我们描述了AKR1C3在胶质瘤和脑膜瘤中的广泛表达,在髓母细胞瘤中表达有限,在神经鞘瘤中不表达。除脑膜瘤外,这些肿瘤通常不被认为是性激素依赖性或相关的脑肿瘤。目前的结果证实了我们先前的观察,即AKR1C3在性激素依赖性和激素非依赖性恶性肿瘤中均有表达。与AKR1C3在肾母细胞瘤中的分布相似,我们也证明了AKR1C3在具有胚胎表型的肿瘤中的表达减少。


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.


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