Breast cancer treatment and sulfotransferase.

Abstract

INTRODUCTION:

Sustained exposure to excessive estrogen is an established risk factor for breast cancer. Sulfotransferase (SULT)-mediated sulfonation represents an effective approach for estrogen deprivation as estrogen sulfates do not bind and activate estrogen receptors (ERs). The nuclear receptor (NR) superfamily functions as a sensor for xenobiotics as well as endogenous molecules, which can regulate the expression of SULT.

AREAS COVERED:

In this review, we summarize the mechanisms of SULT regulation by NRs and inactivation of estrogen by SULT. Furthermore, we discuss the potential of clinical therapy targeting SULT in breast cancer treatment. Gaps in current knowledge that require further study are also highlighted.

EXPERT OPINION:

The prevention of estrogen binding to ER by antiestrogen and inhibition of estrogen synthesis by aromatase or sulfatase inhibitor have been used in clinical therapy for breast cancer. Although the induction of SULT has been proven effective to estrogen inactivation, reports on this method applied to breast cancer treatment are rare. Targeted activation of SULT may open up a new means of treating hormone-dependent breast cancer.

• Authors: Xi-Wei Ji, Tian-Yan Zhou, Yuan Lu, Min-Ji Wei, Wei Lu, William C Cho
• Journal: Expert opinion on therapeutic targets (Expert Opin Ther Targets) Vol. 19 Issue 6 Pg. 821-34 (Jun 2015) ISSN: 1744-7631 [Electronic] England
• PMID: 25677121 (Publication Type: Journal Article, Review)

Chemical References

• Antineoplastic Agents, Hormonal
• Estrogens
• Receptors, Estrogen
• Sulfotransferases

Topics

• Animals
• Antineoplastic Agents, Hormonal (pharmacology)
• Breast Neoplasms (drug therapy, enzymology)
• Drug Design
• Estrogens (metabolism)
• Female
• Humans
• Molecular Targeted Therapy
• Receptors, Estrogen (metabolism)
• Sulfotransferases (metabolism)