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Gene Review

STS  -  steroid sulfatase (microsomal), isozyme S

Homo sapiens

Synonyms: ARSC, ARSC1, ASC, Arylsulfatase C, ES, ...
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Disease relevance of STS

  • Studies have shown that aberrant recombination between arrays of CRI-S232-homologous repeats flanking the steroid sulfatase ( STS ) gene results in STS deletion, which is manifested clinically as X-linked ichthyosis [1].
  • In breast cancer tissues examined by laser capture microdissection/RT-PCR analyses, the mRNA for EST was localized in both carcinoma and intratumoral stromal cells, whereas that of STS was detected only in carcinoma cells [2].
  • EST and STS immunoreactivity was also correlated with various clinicopathological parameters, including prognosis to examine the biological significance of these enzymes in 113 breast carcinomas [2].
  • Of the 113 invasive ductal carcinomas examined in this study, EST and STS immunoreactivity was detected in 50 and 84 cases (44.2 and 74.3%), respectively [2].
  • CONCLUSIONS: STS and EST are expressed and may be involved in local production and metabolism of estrogens in human prostate cancers [3].

Psychiatry related information on STS

  • Identification by STS PCR screening of a microdeletion in Xp21.3-22.1 associated with non-specific mental retardation [4].
  • STS 25 cells express the idiotypic (Id+) immunoglobulin (Ig) specific for the neoplastic B cells of the B-NHL patient [5].
  • Does the Spiritual Transcendence Scale (STS; R. L. Piedmont, 1999) predict psychosocial outcomes from an outpatient substance abuse program [6]?
  • In an attempt to demonstrate the influence of the STS on memory functions in humans, we have investigated the effects of acute administration of exogenous GRF vs. placebo on short-term memory (STM) in healthy young subjects [7].
  • Frequencies of serum groups (Hp and Gc) and red cell enzyme types (PGM1, 6-PGD and ES D) were studied in 195 patients with affective disorders [8].

High impact information on STS

  • We have found that these STS alterations usually involve breakpoints within highly similar sequence elements situated approximately 1.9 megabases apart on the X chromosome [9].
  • Variable deletion breakpoints have been recognized at the alpha-globin and dystrophin loci, but no information is available regarding STS deletions [9].
  • Exceptions in which deletions do account for the majority of observed abnormalities include the alpha-thalassemias, Duchenne muscular dystrophy, and steroid sulfatase deficiency [9].
  • We have cloned and characterized the human STS X-encoded locus and a pseudogene that is present on the long arm of the Y chromosome [10].
  • Human STS is a microsomal enzyme important in steroid metabolism [11].

Chemical compound and disease context of STS


Biological context of STS


Anatomical context of STS

  • STS expression levels were found to be significantly higher in the VSMCs obtained from female aortas with mild atherosclerotic changes than in those with severe atherosclerotic changes and in male aortas regardless of atherosclerotic changes [17].
  • STS activity in freshly isolated cytotrophoblasts was low (about 17%), compared to placental tis- sue, and about 1.7-fold higher in female than in male cells [13].
  • In contrast to the components of the glucose-6-phosphatase system, activity of ARSC in both intact and disrupted microsomes was substantially more resistant to protease inactivation [18].
  • Studies of fibroblast clones from these females provide evidence, presented here, for differential expression of STS loci on the active and inactive X chromosome [19].
  • Further evidence that the STS locus escapes inactivation is that the human inactive X chromosomes contributes STS activity to mouse-human hybrid cells [19].

Associations of STS with chemical compounds


Physical interactions of STS


Regulatory relationships of STS


Other interactions of STS

  • The revelation that CRI-S232 contains VCX offers a more precise description of the genetic etiology of X-linked ichthyosis: it results from aberrant recombination between VCX gene arrays that flank the STS locus [1].
  • The final karyotype was 46,Y,der(X)t(X; Y)(p22.3; q11.2).ish der(X) (DXZ1+, KAL+, STS-, SHOX-) mat [25].
  • We studied the expression of the STS gene in primary cultures of cytotrophoblasts from human term placentae and compared it with the expression of autosomally encoded placental alkaline phosphatase (PALP) and X-linked glucose-6-phosphate dehydrogenase (G6PD) [13].
  • CDPX is located between 2650 and 5550 kb from Xpter, and STS is located between 7250 and 7830 kb from Xpter [26].
  • It is also important to note that the status of intratumoral aromatase, 17beta-HSD type 1, EST and STS in human breast cancer tissues is variable and not necessarily correlated with each other, which suggests different potential sources of intratumoral estrogens among individual patients with breast cancer [20].

Analytical, diagnostic and therapeutic context of STS

  • EST and STS immunoreactivity was detected in carcinoma cells and significantly associated with their mRNA levels (P = 0.0027 and 0.0158, respectively), as measured by RT/real-time PCR, and enzymatic activities (P = 0.0005 and 0.0089, respectively) in 35 breast carcinomas [2].
  • Therefore, in this study, we examined the expression of EST and STS in 35 specimens of human breast carcinoma tissues using immunohistochemistry, reverse transcription-PCR (RT-PCR), and enzymatic assay [2].
  • Western blot analysis using anti-STS antibodies was performed on patients' fibroblast extracts and revealed absence of cross-reacting material [27].
  • However, some patients with the classical XLI phenotype and complete STS deficiency do not show any detectable deletions by Southern blot analysis using full-length STS cDNA as a probe [27].
  • Immunoblotting experiments, performed using anti-STS polyclonal antibodies, revealed the absence of cross-reacting material to STS in all cases tested, including 4 patients without evidence of deletions [28].


  1. A human sex-chromosomal gene family expressed in male germ cells and encoding variably charged proteins. Lahn, B.T., Page, D.C. Hum. Mol. Genet. (2000) [Pubmed]
  2. Estrogen sulfotransferase and steroid sulfatase in human breast carcinoma. Suzuki, T., Nakata, T., Miki, Y., Kaneko, C., Moriya, T., Ishida, T., Akinaga, S., Hirakawa, H., Kimura, M., Sasano, H. Cancer Res. (2003) [Pubmed]
  3. Steroid sulfatase and estrogen sulfotransferase in human prostate cancer. Nakamura, Y., Suzuki, T., Fukuda, T., Ito, A., Endo, M., Moriya, T., Arai, Y., Sasano, H. Prostate (2006) [Pubmed]
  4. Identification by STS PCR screening of a microdeletion in Xp21.3-22.1 associated with non-specific mental retardation. Billuart, P., Vinet, M.C., des Portes, V., Llense, S., Richard, L., Moutard, M.L., Recan, D., Brüls, T., Bienvenu, T., Kahn, A., Beldjord, C., Chelly, J. Hum. Mol. Genet. (1996) [Pubmed]
  5. Functional and molecular characterization of B cell line derived interleukin-1 alpha. Vyth-Dreese, F.A., Hekman, A., Wijffels, J., Geertsma, M., Dellemijn, T.A., Dosda, J., Melief, C.J., Bertoglio, J. Leukemia (1989) [Pubmed]
  6. Spiritual transcendence as a predictor of psychosocial outcome from an outpatient substance abuse program. Piedmont, R.L. Psychology of addictive behaviors : journal of the Society of Psychologists in Addictive Behaviors. (2004) [Pubmed]
  7. Effects of GRF (1-29) NH2 on short-term memory: neuroendocrine and neuropsychological assessment in healthy young subjects. Alvarez, X.A., Cacabelos, R. Methods and findings in experimental and clinical pharmacology. (1990) [Pubmed]
  8. Serum protein and red cell enzyme polymorphisms in affective disorders. Beckman, G., Beckman, L., Cedergren, B., Perris, C., Strandman, E. Hum. Hered. (1978) [Pubmed]
  9. Frequent deletions of the human X chromosome distal short arm result from recombination between low copy repetitive elements. Yen, P.H., Li, X.M., Tsai, S.P., Johnson, C., Mohandas, T., Shapiro, L.J. Cell (1990) [Pubmed]
  10. The human X-linked steroid sulfatase gene and a Y-encoded pseudogene: evidence for an inversion of the Y chromosome during primate evolution. Yen, P.H., Marsh, B., Allen, E., Tsai, S.P., Ellison, J., Connolly, L., Neiswanger, K., Shapiro, L.J. Cell (1988) [Pubmed]
  11. Cloning and expression of steroid sulfatase cDNA and the frequent occurrence of deletions in STS deficiency: implications for X-Y interchange. Yen, P.H., Allen, E., Marsh, B., Mohandas, T., Wang, N., Taggart, R.T., Shapiro, L.J. Cell (1987) [Pubmed]
  12. Steroid sulfatase and estrogen sulfotransferase in normal human tissue and breast carcinoma. Suzuki, T., Miki, Y., Nakata, T., Shiotsu, Y., Akinaga, S., Inoue, K., Ishida, T., Kimura, M., Moriya, T., Sasano, H. J. Steroid Biochem. Mol. Biol. (2003) [Pubmed]
  13. Differential increase of steroid sulfatase activity in XX and XY trophoblast cells from human term placenta with syncytia formation in vitro. Ugele, B., Regemann, K. Cytogenet. Cell Genet. (2000) [Pubmed]
  14. Large-insert clone/STS contigs in Xq11-q12, spanning deletions in patients with androgen insensitivity and mental retardation. Schueler, M.G., Higgins, A.W., Nagaraja, R., Tentler, D., Dahl, N., Gustashaw, K., Willard, H.F. Genomics (2000) [Pubmed]
  15. Low maternal serum unconjugated estriol during prenatal screening as an indication of placental steroid sulfatase deficiency and X-linked ichthyosis. Keren, D.F., Canick, J.A., Johnson, M.Z., Schaldenbrand, J.D., Haning, R.V., Hackett, R. Am. J. Clin. Pathol. (1995) [Pubmed]
  16. Quantitative analysis of aromatase, sulfatase and 17beta-HSD(1) mRNA expression in soft tissue metastases of breast cancer. Irahara, N., Miyoshi, Y., Taguchi, T., Tamaki, Y., Noguchi, S. Cancer Lett. (2006) [Pubmed]
  17. Steroid sulfatase and estrogen sulfotransferase in the atherosclerotic human aorta. Nakamura, Y., Miki, Y., Suzuki, T., Nakata, T., Darnel, A.D., Moriya, T., Tazawa, C., Saito, H., Ishibashi, T., Takahashi, S., Yamada, S., Sasano, H. Am. J. Pathol. (2003) [Pubmed]
  18. Microsomal steroid sulfatase: interactions with cytosolic steroid sulfotransferases. Kauffman, F.C., Sharp, S., Allan, B.B., Burchell, A., Coughtrie, M.W. Chem. Biol. Interact. (1998) [Pubmed]
  19. Differential expression of steroid sulphatase locus on active and inactive human X chromosome. Migeon, B.R., Shapiro, L.J., Norum, R.A., Mohandas, T., Axelman, J., Dabora, R.L. Nature (1982) [Pubmed]
  20. New development in intracrinology of breast carcinoma. Sasano, H., Suzuki, T., Nakata, T., Moriya, T. Breast Cancer (2006) [Pubmed]
  21. Cloning and expression of human steroid-sulfatase. Membrane topology, glycosylation, and subcellular distribution in BHK-21 cells. Stein, C., Hille, A., Seidel, J., Rijnbout, S., Waheed, A., Schmidt, B., Geuze, H., von Figura, K. J. Biol. Chem. (1989) [Pubmed]
  22. Complex RNA processing of TDRKH, a novel gene encoding the putative RNA-binding tudor and KH domains. Lamb, F.S., Barna, T.J., Goud, C., Marenholz, I., Mischke, D., Schutte, B.C. Gene (2000) [Pubmed]
  23. A specific ultrastructural stain for arylsulfatase A activity in human cultured fibroblasts. Chang, P.L., Moudgil, G. J. Histochem. Cytochem. (1984) [Pubmed]
  24. Retinoid-mediated stimulation of steroid sulfatase activity in myeloid leukemic cell lines requires RARalpha and RXR and involves the phosphoinositide 3-kinase and ERK-MAP kinase pathways. Hughes, P.J., Zhao, Y., Chandraratna, R.A., Brown, G. J. Cell. Biochem. (2006) [Pubmed]
  25. An Xp; Yq translocation causing a novel contiguous gene syndrome in brothers with generalized epilepsy, ichthyosis, and attention deficits. Doherty, M.J., Glass, I.A., Bennett, C.L., Cotter, P.D., Watson, N.F., Mitchell, A.L., Bird, T.D., Farrell, D.F. Epilepsia (2003) [Pubmed]
  26. Long-range restriction map of the terminal part of the short arm of the human X chromosome. Petit, C., Levilliers, J., Weissenbach, J. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  27. Identification of point mutations in the steroid sulfatase gene of three patients with X-linked ichthyosis. Basler, E., Grompe, M., Parenti, G., Yates, J., Ballabio, A. Am. J. Hum. Genet. (1992) [Pubmed]
  28. Molecular heterogeneity of steroid sulfatase deficiency: a multicenter study on 57 unrelated patients, at DNA and protein levels. Ballabio, A., Carrozzo, R., Parenti, G., Gil, A., Zollo, M., Persico, M.G., Gillard, E., Affara, N., Yates, J., Ferguson-Smith, M.A. Genomics (1989) [Pubmed]
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