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• W1209997289 abstract "Objective To study the influences of endocannabinoid-anandamide （AEA） on the proliferation and apoptosis of the colorectal cancer cell line （CaCo-2） and to elucidate the effects of CBI and lipid rafts, and to further elucidate the molecular mechanism and the effect of AEA on the generation and development of colorectal cancer. Methods Human eolorectal cancer cell line CaCo-2 was cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum in 5% CO2 atmosphere at 37℃. CaCo-2 cells were divided into different groups and treated with different concentrations of AEA, AEA ＋ SRI41716A, AEA ＋ AM630 and AEA ＋ methyl-β-cyclodextrin （MCD）. MTI＂ assay was used to determine the effects of AEA, its putative CBI, CB2 receptor antagonists （SR141716A and AM630） and MCD on the proliferation of CaCo-2 cells. Annexin V-PE/7AAD binding assay was used to detect apoptosis in the CaCo-2 cells. Western-blot was applied to check the expressions of CBI, CB2, p-AKT and caspase-3 proteins in different groups of CaCo-2 ceils. Results AEA inhibited the proliferation of CaCo-2 cells in a concentrationdependent manner and the effect could be antagonized by SR141716A and MCD. The inhibiting rates were （21.52±0.45）%, （42. 16±0.21）%, （73.64±0.73）% and（83.28 ±0.71）%, respectively, at different concentrations of AEA （5, 10, 20 and 40 μmol/L）. The three groups （20 μmol/L AEA, 20μmol/L AEA ＋ 10 μmol/L SR141716A and 20 p,mol/L AEA ＋ 1 mmol/L MCD） showed different inhibiting rates[ （73.64 ±0.73）%, （ 16. 15 ± 0.75）% and （ 12.58 ±0.63）% ], respectively. Annexin V-PE/7AAD binding assay showed that AEA induced apoptosis in the CaCo-2 cells and MCD could antagonize this effect. The apoptosis rates of the three groups （ control, 20 gtmol/L AEA and 20 Ixrnol/L AEA ＋ 1 mmol/L MCD） were （2.95 ± 0.73 ） % , （39.61 ± 0.73 ） % and （ 14.10 ± 0.64） % , respectively. The expressions of CBI, CB2, p-AKT and Caspase-3 proteins were all observed in the CaCo-2 cells. AEA inhibited p-AKT protein expression and induced caspase-3 protein expression. The two actions were also antagonized by MCD. Conclusions AEA can strongly suppress the proliferation of colorectal cancer CaCo-2 cells via the CBI receptor and membrane eholesterol-LRs and induce apoptosis via lipid rafts. Anandamide plays a very important role in the carcinogenesis and development of colorectal cancer. MCD is a critical member in this system.Key words: Anandamide;  Colonic neoplasms;  CaCo-2 cells;  Lipid rafts;  CB1" @default.
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• W1209997289 date "2011-04-01" @default.
• W1209997289 modified "2023-09-25" @default.
• W1209997289 title "Anandamide inhibits the growth of colorectal cancer cells through CB1 and lipid rafts" @default.
• W1209997289 doi "https://doi.org/10.3760/cma.j.issn.0253-3766.2011.04.004" @default.
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