Biological and Pharmaceutical Bulletin
Online ISSN : 1347-5215
Print ISSN : 0918-6158
ISSN-L : 0918-6158
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Δ9-Tetrahydrocannabinol Targeting Estrogen Receptor Signaling: The Possible Mechanism of Action Coupled with Endocrine Disruption
Shuso Takeda
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2014 Volume 37 Issue 9 Pages 1435-1438

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Abstract

Δ9-Tetrahydrocannabinol (Δ9-THC), a biologically active constituent of marijuana, possesses a wide variety of pharmacological and toxicological effects (e.g., analgesia, hypotension, reduction of inflammation, and anti-cancer effects). Among Δ9-THC’s biological activities, its recognized anti-estrogenic activity has been the subject of investigations. Since Δ9-THC is used as both a drug of abuse (marijuana) and as a preventive therapeutic to treat pain and nausea in cancer patients undergoing chemotherapy in the United States and other countries (synthesized Δ9-THC; dronabinol), it is important to investigate the mechanistic basis underlying the anti-estrogenic activity of Δ9-THC. Since Δ9-THC has “no” binding potential for estrogen receptor α (ERα) which can be activated by estrogen (E2), the question of how Δ9-THC exerts its inhibitory effect on ERα is not resolved. We have recently reported that ERβ, a second type of ER, is involved in the Δ9-THC abrogation of E2/ERα-mediated transcriptional activity. Here we discuss the possible mechanism(s) of the Δ9-THC-mediated disruption of E2/ERα signaling by presenting our recent findings as well.

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© 2014 The Pharmaceutical Society of Japan
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