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Delta(9)-Tetrahydrocannabinol enhances MCF-7 cell proliferation via cannabinoid receptor-independent signaling.
Toxicology. 2008 Mar 12; 245(1-2):141-6.T

Abstract

We recently reported that Delta(9)-tetrahydrocannabinol (Delta(9)-THC) has the ability to stimulate the proliferation of human breast carcinoma MCF-7 cells. However, the mechanism of action remains to be clarified. The present study focused on the relationship between receptor expression and the effects of Delta(9)-THC on cell proliferation. RT-PCR analysis demonstrated that there was no detectable expression of CB receptors in MCF-7 cells. In accordance with this, no effects of cannabinoid 1/2 (CB1/2) receptor antagonists and pertussis toxin on cell proliferation were observed. Although MCF-7 cell proliferation is suggested to be suppressed by Delta(9)-THC in the presence of CB receptors, it was revealed that Delta(9)-THC could exert upregulation of living cells in the absence of the receptors. Interestingly, Delta(9)-THC upregulated human epithelial growth factor receptor type 2 (HER2) expression, which is known to be a predictive factor of human breast cancer and is able to stimulate cancer cells as well as MCF-7 cells. Actinomycin D-treatment interfered with the upregulation of HER2 and cell proliferation by cannabinoid. Taken together, these studies suggest that, in the absence of CB receptors, Delta(9)-THC can stimulate the proliferation of MCF-7 cells by modulating, at least in part, HER2 transcription.

Authors+Show Affiliations

Organization for Frontier Research in Preventive Pharmaceutical Sciences, Hokuriku University, Ho-3 Kanagawa-machi, Kanazawa 920-1181, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18249480

Citation

Takeda, Shuso, et al. "Delta(9)-Tetrahydrocannabinol Enhances MCF-7 Cell Proliferation Via Cannabinoid Receptor-independent Signaling." Toxicology, vol. 245, no. 1-2, 2008, pp. 141-6.
Takeda S, Yamaori S, Motoya E, et al. Delta(9)-Tetrahydrocannabinol enhances MCF-7 cell proliferation via cannabinoid receptor-independent signaling. Toxicology. 2008;245(1-2):141-6.
Takeda, S., Yamaori, S., Motoya, E., Matsunaga, T., Kimura, T., Yamamoto, I., & Watanabe, K. (2008). Delta(9)-Tetrahydrocannabinol enhances MCF-7 cell proliferation via cannabinoid receptor-independent signaling. Toxicology, 245(1-2), 141-6. https://doi.org/10.1016/j.tox.2007.12.019
Takeda S, et al. Delta(9)-Tetrahydrocannabinol Enhances MCF-7 Cell Proliferation Via Cannabinoid Receptor-independent Signaling. Toxicology. 2008 Mar 12;245(1-2):141-6. PubMed PMID: 18249480.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Delta(9)-Tetrahydrocannabinol enhances MCF-7 cell proliferation via cannabinoid receptor-independent signaling. AU - Takeda,Shuso, AU - Yamaori,Satoshi, AU - Motoya,Erina, AU - Matsunaga,Tamihide, AU - Kimura,Toshiyuki, AU - Yamamoto,Ikuo, AU - Watanabe,Kazuhito, Y1 - 2007/12/28/ PY - 2007/11/07/received PY - 2007/12/17/revised PY - 2007/12/18/accepted PY - 2008/2/6/pubmed PY - 2008/4/29/medline PY - 2008/2/6/entrez SP - 141 EP - 6 JF - Toxicology JO - Toxicology VL - 245 IS - 1-2 N2 - We recently reported that Delta(9)-tetrahydrocannabinol (Delta(9)-THC) has the ability to stimulate the proliferation of human breast carcinoma MCF-7 cells. However, the mechanism of action remains to be clarified. The present study focused on the relationship between receptor expression and the effects of Delta(9)-THC on cell proliferation. RT-PCR analysis demonstrated that there was no detectable expression of CB receptors in MCF-7 cells. In accordance with this, no effects of cannabinoid 1/2 (CB1/2) receptor antagonists and pertussis toxin on cell proliferation were observed. Although MCF-7 cell proliferation is suggested to be suppressed by Delta(9)-THC in the presence of CB receptors, it was revealed that Delta(9)-THC could exert upregulation of living cells in the absence of the receptors. Interestingly, Delta(9)-THC upregulated human epithelial growth factor receptor type 2 (HER2) expression, which is known to be a predictive factor of human breast cancer and is able to stimulate cancer cells as well as MCF-7 cells. Actinomycin D-treatment interfered with the upregulation of HER2 and cell proliferation by cannabinoid. Taken together, these studies suggest that, in the absence of CB receptors, Delta(9)-THC can stimulate the proliferation of MCF-7 cells by modulating, at least in part, HER2 transcription. SN - 0300-483X UR - https://www.unboundmedicine.com/medline/citation/18249480/Delta_9__Tetrahydrocannabinol_enhances_MCF_7_cell_proliferation_via_cannabinoid_receptor_independent_signaling_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0300-483X(07)00856-6 DB - PRIME DP - Unbound Medicine ER -