Characterization of 17β-Hydroxysteroid Dehydrogenase Activity and mRNA Abundance in Human Meningioma Tumors

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Abstract
Meningioma benign tumors possess significant levels of 17β-hydroxysteroid dehydrogenase (17β-HSD) activity. Two different 17β-HSDs have been cloned and characterized. The cytosolic 17β-HSD I which exclusively catalyzes the interconversion of 17β-estradiol (E2) and estrone (E1) preferentially uses NADP+ and NADPH as cofactors. In contrast, the mitochondrial-microsomal 17β-HSD II catalyzes both the estrogenic as well as the androgenic substrates of the 17β-HSD and uses NAD+ and NADH as cofactors. We demonstrated here that the 17β-HSD activity in meningioma tissue homogenate is both estrogenic and androgenic with Km values of 2.4, 0.4, 14.7, and 2.0 µM for E2, E1, testosterone (T), and Δ4-androstenedione (Δ4), respectively. NAD+-NADH is almost exclusively used as cofactor in this tissue. Moreover, fractionation of meningioma tissue revealed that most of the 17β-HSD activity is present in the mitochondrial-microsomal fraction. Although Northern blot analysis on meningiomas with a specific probe for human 17β-HSD I showed no band, the specific cDNA probe of human 17β-HSD II hybridized at the expected size of 1.5 kb, which was also present in placenta. On four different meningioma tumors, we were able to correlate 17β-HSD II mRNA expression to high levels of 17β-HSD activity. Taken together, the present data suggest that the meningioma 17β-HSD could be the 17β-HSD II.

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