- Hironori Aramaki (Department of Molecular Biology, Daiichi University of Pharmacy / Drug Innovation Research Center, Daiichi University of Pharmacy / firstname.lastname@example.org)
1) Department of Molecular Biology, Daiichi University of Pharmacy , 2) Laboratory of Xenobiotic Metabolism and Environmental Toxicology, Faculty of Pharmaceutical Sciences, Hiroshima International University (HIU) , 3) Department of Hygienic Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University , 4) Drug Innovation Research Center, Daiichi University of Pharmacy
Δ9-Tetrahydrocannabinol (Δ9-THC), an active ingredient of marijuana, evokes a number of biological effects including anti-cancer and anti-estrogenic actions. We and others have so far focused on and investigated the latter action. We recently reported that Δ9-THC up-regulates the expression of estrogen receptor β (ERβ, ESR2), resulting in the abrogation of 17β-estradiol (E2)-mediated ERα signaling (Takeda et al., Chem. Res. Toxicol., 26, 1073-1079, 2013). This finding may shed light on the possible endocrine-disrupting mechanism(s) employed by cannabinoids including Δ9-THC. Although previous studies have suggested that HU-210, a synthetic analog of Δ9-THC, evokes a set of endocrine alterations closely related to those of Δ9-THC, none have examined the effects of cannabinoids with a focus on the expression of ERβ, a “suppressive” molecule for ERα-mediated signaling. Thus, we herein determined whether HU-210 is also an endocrine modifier similar to Δ9-THC using ERα-positive MCF-7 cells in which the expression of ERβ is maintained at very low levels. The results of the present study revealed that HU-210, despite having a similar structure to Δ9-THC, did not modulate E2/ERα signaling or induce ERβ.