Estrone sulfatase activity in normal and abnormal endometrium

Abstract

We investigated the activity of estrone sulfatase in normal and pathological endometrium. In normal endometrium, the estrone sulfatase activity [pmol E1 X min-1 X (mg prot)-1] was 23.13 +/- 8.44 (mean +/- SD). An increase (p less than 0.01) of estrone sulfatase activity (62.81 +/- 21.97) was noted in mild endometrial hyperplasia. In focal hyperplasia (when the measurements were performed in the normal endometrial biopsies) such an increase was not noted (19.10 +/- 5.33). Estrone sulfatase activities of moderate hyperplasia (25.30 +/- 11.40) and endometrial neoplasia (30.30 +/- 9.57) were in the same range as in normal endometrium. Treatment with progestagen simultaneously reduced hyperplasia and estrone sulfatase activity. But when morphologically abnormal endometrium persisted after treatment, estrone sulfatase activity remained increased. The increase of estrone sulfatase activity appeared to be specific to mild endometrial hyperplasia. The role of estrone sulfatase in the pathogenesis of endometrial hyperplasia is discussed.

Steroid Sulfatase: Molecular Biology, Regulation, and Inhibition

“…STS activity has been detected in normal and hyperplastic endometrial tissues (161). It has been suggested that uterine STS activity may have an important role in regulating the uterotropic activity of E2S (162).…”

The Important Roles of Steroid Sulfatase and Sulfotransferases in Gynecological Diseases

“…At the cellular level, STS immunoreactivity in endometrial cancer tissue was higher compared to normal endometrium (Utsunomiya et al, 2004 ), which suggests increased availability of the biologically active estrogens. In line with this, immunohistochemical data and early metabolism studies have shown significantly higher E1-S STS activity in endometrial cancer tissue, compared to control endometrium (Adessi et al, 1984 ; Prost et al, 1984 ; Naitoh et al, 1989 ; Urabe et al, 1989 ). However, more recently, Tanaka et al reported lower E1-S STS activity in cancerous tissue, compared to normal endometrium (Tanaka et al, 2003 ).…”

“…There is a plethora of data that supports the important role of STS in individual gynecological diseases, with disturbances reported for the balance between the STS and SULT enzymes. Although the observed STS mRNA and protein levels were rarely increased, higher STS activities have been seen in the majority of pathological tissues and in model cell lines, including cancerous endometrium (Adessi et al, 1984 ; Prost et al, 1984 ; Naitoh et al, 1989 ; Urabe et al, 1989 ; Day et al, 2009 ), ovarian cancer cell lines (Day et al, 2009 ; Ren et al, 2015 ), and adenomyosis (Yamamoto et al, 1993 ; Ezaki et al, 2001 ). This is in line with the higher catalytic efficiency of STS vs. SULT (Table 1 ), and in some cases, higher expression levels of STS (Tables 3 , 6 ).…”

Specific effect of oestrone sulphate on protein synthesis and secretion by cultured epithelial cells from guinea-pig endometrium

“…Adessi et al (1982) have described a plausible role of prehormone for oestrogen sulphates in the guinea-pig uterus and Moutaouakkil et al (1984) have postulated that the variation in oestrone sulphatase activity in the guinea-pig uterus could control the intracellular levels of biologically active oestrogens. The human uterus is able to convert sulphated oestrogens into unconjugated ones and the formation of oestradiol-17ß from oestrone sulphate in human endometrium could be of importance in the genesis of endometrial disorders Adessi, Prost, Agnani et al 1984;Carlström, Bergqvist & Ljungberg, 1988). The oestrogenic effect of oestrone sulphate was attributed to its intracellular transformation into unconjugated oestradiol-17ß and its action considered to be mimicking that of this potent oestrogen.…”