硫酸酯酶（STS）和磺基转移酶（SULT）在类固醇激素的生物合成和作用中具有重要作用。 STS 催化硫酸雌酮 (E1-S) 和硫酸脱氢表雄酮 (DHEA-S) 的水解，而磺基转移酶催化逆反应并需要 3-磷酸腺苷-5-磷酸硫酸盐作为硫酸盐供体。这些酶控制外周组织中活性雌激素和雄激素的浓度。在良性激素依赖性疾病和激素依赖性癌症中都发现了 STS 和 SULT 基因的异常表达。本综述的目的是介绍目前关于 STS 和 SULT 在妇科癌症、子宫内膜癌 (EC) 和卵巢癌 (OC) 中的作用的知识。 EC 是最常见的妇科癌症，OC 是最致命的妇科癌症。这些癌症主要影响绝经后妇女，因此依赖于非活性前体（DHEA-S 或 E1-S）在局部产生类固醇激素。在有机阴离子转运多肽 (OATP) 或有机阴离子转运蛋白 (OAT) 被细胞摄取后，STS 和 SULT 调节活性雌激素和雄激素的形成，因此 STS 和 SULT 之间的平衡紊乱可能导致癌症的发生和进展。这些酶在外周雌激素生物合成中的重要性早已得到认可，这篇综述提供了关于 STS 和 SULT 在雄激素形成和作用中的重要作用、它们的调节和抑制以及它们作为预后生物标志物的潜力的新数据。© 2024作者。

Sulfatase (STS) and sulfotransferases (SULT) have important role in the biosynthesis and action of steroid hormones. STS catalyzes the hydrolysis of estrone-sulfate (E1-S) and dehydroepiandrosterone-sulfate (DHEA-S), while sulfotransferases catalyze the reverse reaction and require 3-phosphoadenosine-5-phosphosulfate as a sulfate donor. These enzymes control the concentration of active estrogens and androgens in peripheral tissues. Aberant expression of STS and SULT genes has been found in both, benign hormone-dependent diseases and hormone-dependent cancers. The aim of this review is to present the current knowledge on the role of STS and SULT in gynecological cancers, endometrial (EC) and ovarian cancer (OC). EC is the most common and OC the most lethal gynecological cancer. These cancers primarily affect postmenopausal women and therefore rely on the local production of steroid hormones from inactive precursors, either DHEA-S or E1-S. Following cellular uptake by organic anion transporting polypeptides (OATP) or organic anion transporters (OAT), STS and SULT regulate the formation of active estrogens and androgens, thus disturbed balance between STS and SULT can contribute to the onset and progression of cancer. The importance of these enzymes in peripheral estrogen biosynthesis has long been recognized, and this review provides new data on the important role of STS and SULT in the formation and action of androgens, their regulation and inhibition, and their potential as prognostic biomarkers.© 2024 The Author(s).