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Antiproliferative mechanism of a cannabinoid agonist by cell cycle arrest in human gastric cancer cells.
J Cell Biochem. 2011 Apr; 112(4):1192-205.JC

Abstract

For gastric cancers, the antineoplastic activity of cannabinoids has been investigated in only a few reports and knowledge regarding the mechanisms involved is limited. We have reported previously that treatment of gastric cancer cells with a cannabinoid agonist significantly decreased cell proliferation and induced apoptosis. Here, we evaluated the effects of cannabinoids on various cellular mediators involved in cell cycle arrest in gastric cancer cells. AGS and MKN-1 cell lines were used as human gastric cancer cells and WIN 55,212-2 as a cannabinoid agonist. Cell cycles were analyzed by flow cytometry and western blotting. Treatment with WIN 55,212-2 arrested the cell cycle in the G0/G1 phase. WIN 55,212-2 also upregulated phospho-ERK1/2, induced Kip1/p27 and Cip1/WAF1/p21 expression, decreased cyclin D1 and cyclin E expression, decreased Cdk 2, Cdk 4, and Cdk 6 expression levels, and decreased phospho-Rb and E2F-1 expression. ERK inhibitor decreased the proportion of G0/G1 phase which was induced by WIN 55,212-2. Inhibition of pAKT led to cell cycle arrest in gastric cancer cells. Cell cycle arrest preceded apoptotic response. Thus, this cannabinoid agonist can reduce gastric cancer cell proliferation via G1 phase cell cycle arrest, which is mediated via activation of the MAPK pathway and inhibition of pAKT.

Authors+Show Affiliations

Division of Gastroenterology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.No affiliation info availableNo 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

21312237

Citation

Park, Jae Myung, et al. "Antiproliferative Mechanism of a Cannabinoid Agonist By Cell Cycle Arrest in Human Gastric Cancer Cells." Journal of Cellular Biochemistry, vol. 112, no. 4, 2011, pp. 1192-205.
Park JM, Xian XS, Choi MG, et al. Antiproliferative mechanism of a cannabinoid agonist by cell cycle arrest in human gastric cancer cells. J Cell Biochem. 2011;112(4):1192-205.
Park, J. M., Xian, X. S., Choi, M. G., Park, H., Cho, Y. K., Lee, I. S., Kim, S. W., & Chung, I. S. (2011). Antiproliferative mechanism of a cannabinoid agonist by cell cycle arrest in human gastric cancer cells. Journal of Cellular Biochemistry, 112(4), 1192-205. https://doi.org/10.1002/jcb.23041
Park JM, et al. Antiproliferative Mechanism of a Cannabinoid Agonist By Cell Cycle Arrest in Human Gastric Cancer Cells. J Cell Biochem. 2011;112(4):1192-205. PubMed PMID: 21312237.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Antiproliferative mechanism of a cannabinoid agonist by cell cycle arrest in human gastric cancer cells. AU - Park,Jae Myung, AU - Xian,Xiang-Shu, AU - Choi,Myung-Gyu, AU - Park,Hyeyeon, AU - Cho,Yu Kyung, AU - Lee,In Seok, AU - Kim,Sang Woo, AU - Chung,In-Sik, PY - 2011/2/12/entrez PY - 2011/2/12/pubmed PY - 2011/8/2/medline SP - 1192 EP - 205 JF - Journal of cellular biochemistry JO - J Cell Biochem VL - 112 IS - 4 N2 - For gastric cancers, the antineoplastic activity of cannabinoids has been investigated in only a few reports and knowledge regarding the mechanisms involved is limited. We have reported previously that treatment of gastric cancer cells with a cannabinoid agonist significantly decreased cell proliferation and induced apoptosis. Here, we evaluated the effects of cannabinoids on various cellular mediators involved in cell cycle arrest in gastric cancer cells. AGS and MKN-1 cell lines were used as human gastric cancer cells and WIN 55,212-2 as a cannabinoid agonist. Cell cycles were analyzed by flow cytometry and western blotting. Treatment with WIN 55,212-2 arrested the cell cycle in the G0/G1 phase. WIN 55,212-2 also upregulated phospho-ERK1/2, induced Kip1/p27 and Cip1/WAF1/p21 expression, decreased cyclin D1 and cyclin E expression, decreased Cdk 2, Cdk 4, and Cdk 6 expression levels, and decreased phospho-Rb and E2F-1 expression. ERK inhibitor decreased the proportion of G0/G1 phase which was induced by WIN 55,212-2. Inhibition of pAKT led to cell cycle arrest in gastric cancer cells. Cell cycle arrest preceded apoptotic response. Thus, this cannabinoid agonist can reduce gastric cancer cell proliferation via G1 phase cell cycle arrest, which is mediated via activation of the MAPK pathway and inhibition of pAKT. SN - 1097-4644 UR - https://www.unboundmedicine.com/medline/citation/21312237/Antiproliferative_mechanism_of_a_cannabinoid_agonist_by_cell_cycle_arrest_in_human_gastric_cancer_cells_ L2 - https://doi.org/10.1002/jcb.23041 DB - PRIME DP - Unbound Medicine ER -