ArticleChemical research in toxicology2013
Δ(9)-Tetrahydrocannabinol disrupts estrogen-signaling through up-regulation of estrogen receptor β (ERβ).
Article in Chemical research in toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 62 citations in OpenAlex.
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- Role of CB1 Cannabinoid Receptors in Vascular Responses and Vascular Remodeling of the Aorta in Female Mice.International journal of molecular sciences · 2023Article
- Sex differences in endocannabinoid tone in a pilot study of cannabis use disorder and acute cannabis abstinence.Addiction biology · 2023Article
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- Cannabis with breast cancer treatment: propitious or pernicious?3 Biotech · 2022Article
- Persistent sexually dimorphic effects of adolescent THC exposure on hippocampal synaptic plasticity and episodic memory in rodents.Neurobiology of disease · 2022Article
- Cannabinoids in Breast Cancer: Differential Susceptibility According to Subtype.Molecules (Basel, Switzerland) · 2021Review
- Environment, Lifestyle, and Female Infertility.Reproductive sciences (Thousand Oaks, Calif.) · 2021Review
- The Complex Interplay between Endocannabinoid System and the Estrogen System in Central Nervous System and Periphery.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Δ(9)-Tetrahydrocannabinol (Δ(9)-THC) has been reported as possessing antiestrogenic activity, although the mechanisms underlying these effects are poorly delineated. In this study, we used the estrogen receptor α (ERα)-positive human breast cancer cell line, MCF-7, as an experimental model and showed that Δ(9)-THC exposures markedly suppresses 17β-estradiol (E2)- induced MCF-7 cell proliferation. We demonstrate that these effects result from Δ(9)-THC's ability to inhibit E2-liganded ERα activation. Mechanistically, the data obtained from biochemical analyses revealed that (i) Δ(9)-THC up-regulates ERβ, a repressor of ERα, inhibiting the expression of E2/ERα-regulated genes that promote cell growth and that (ii) Δ(9)-THC induction of ERβ modulates E2/ERα signaling in the absence of direct interaction with the E2 ligand binding site. Therefore, the data presented support the concept that Δ(9)-THC's antiestrogenic activities are mediated by the ERβ disruption of E2/ERα signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.