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Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
Breast cancer treatment and sulfotransferase
Xi-Wei Ji1, Tian-Yan Zhou, Yuan Lu
1Institute of Clinical Pharmacology, Peking University First Hospital, Peking University , Beijing , China jjxxeezz@163.com.
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.
Insights
Targeting sulfotransferase (SULT) enzymes offers a novel strategy for breast cancer treatment by inactivating estrogen. Activating SULT may provide a new therapeutic avenue for hormone-dependent breast cancer.
Area of Science:
- Biochemistry
- Endocrinology
- Oncology
Background:
- Excessive estrogen exposure is a known breast cancer risk factor.
- Sulfotransferase (SULT)-mediated sulfonation inactivates estrogen, preventing estrogen receptor (ER) activation.
- Nuclear receptors (NRs) regulate SULT expression, sensing endogenous and xenobiotic molecules.
Purpose of the Study:
- To review SULT regulation by NRs and estrogen inactivation mechanisms.
- To discuss the potential of SULT-targeted therapies for breast cancer.
- To identify knowledge gaps for future research.
Main Methods:
- Review of literature on SULT regulation by NRs.
- Summary of estrogen inactivation pathways mediated by SULT.
- Discussion of clinical applications and future research directions.
Main Results:
- NRs play a key role in regulating SULT-mediated estrogen inactivation.
- SULT induction is an effective method for estrogen inactivation.
- Clinical application of SULT induction for breast cancer treatment is underexplored.
Conclusions:
- Targeted activation of SULT presents a promising new therapeutic strategy for hormone-dependent breast cancer.
- Further research is needed to explore the clinical efficacy of SULT-targeted therapies.
- This approach offers an alternative to current antiestrogen and estrogen synthesis inhibitors.
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