Effects of Blue-I,a metabolite from marine Rhodomarinobacter spp. on proliferation of human gastric cancer cells
Bao Yuan
Abstract
Bao Yuan
Abstract
AIM To study whether Blue-Ⅰ3-[1,2-dihydro-5-(5-hydroxy-1H-indol-3-yl-)-2-oxo-2h-pyrrol-3-ylidene]-1,3-dihydro-2H-indol-2-one, a metabolic product from a new marine species, Rhodomarinobacter spp. inhibits proliferation of human gastric cancer cells(MCG803). METHODS The IC_ 50 of Blue-Ⅰ on MCG803 was determined by MTT test. DNA damage was detected by single cell electrophoresis . Apoptosis cells and the cell cycles of tumor cells were analyzed by Hoechst 33258 staining and by flow cytometer assay. RESULTS The MCG803 cell proliferation was inhibited by Blue-Ⅰ and the IC_ 50 was (4.6±1.1)mg·L~ -1 . The degradation of the genome of the apoptotic cells induced by the Blue-Ⅰ was also detected.The percentage of tailed cells were (23.2±4.9)%,(51.4± 6.9)% and (68.7±6.5)% in the groups containing 2.5, 5 and 10 mg·L~ -1 of Blue-Ⅰ, respectively, while (4.2± 1.2)% in the control group. The average tail length increased with the concentrations of Blue-Ⅰ detected with comet assay. When MCG803 cells were treated with 2.5-10 mg·L~ -1 Blue-Ⅰ for 24 h, the typical apoptotic nuclear morphological changes were observed with Hoechst 33258 staining. The ratios of the apoptotic cells were (11.4±3.5) %, (32.4±4.9 )% and (50.7±6.6)% in the groups containing 2.5, 5 and 10 mg·L~ -1 of Blue-Ⅰ respectively, as compared with(3.5±0.6)% in the untreated group. Flow cytometry assay indicated that the cell cycles of the tumor cells were also altered by the compound. CONCLUSION Blue-Ⅰ could effectively suppress the gastric cancer cells proliferation. The mechanism perhaps involved in the apoptosis of gastric cancer cells induced by Blue-Ⅰ.
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AIM To study whether Blue-Ⅰ3-[1,2-dihydro-5-(5-hydroxy-1H-indol-3-yl-)-2-oxo-2h-pyrrol-3-ylidene]-1,3-dihydro-2H-indol-2-one, a metabolic product from a new marine species, Rhodomarinobacter spp. inhibits proliferation of human gastric cancer cells(MCG803). METHODS The IC_ 50 of Blue-Ⅰ on MCG803 was determined by MTT test. DNA damage was detected by single cell electrophoresis . Apoptosis cells and the cell cycles of tumor cells were analyzed by Hoechst 33258 staining and by flow cytometer assay. RESULTS The MCG803 cell proliferation was inhibited by Blue-Ⅰ and the IC_ 50 was (4.6±1.1)mg·L~ -1 . The degradation of the genome of the apoptotic cells induced by the Blue-Ⅰ was also detected.The percentage of tailed cells were (23.2±4.9)%,(51.4± 6.9)% and (68.7±6.5)% in the groups containing 2.5, 5 and 10 mg·L~ -1 of Blue-Ⅰ, respectively, while (4.2± 1.2)% in the control group. The average tail length increased with the concentrations of Blue-Ⅰ detected with comet assay. When MCG803 cells were treated with 2.5-10 mg·L~ -1 Blue-Ⅰ for 24 h, the typical apoptotic nuclear morphological changes were observed with Hoechst 33258 staining. The ratios of the apoptotic cells were (11.4±3.5) %, (32.4±4.9 )% and (50.7±6.6)% in the groups containing 2.5, 5 and 10 mg·L~ -1 of Blue-Ⅰ respectively, as compared with(3.5±0.6)% in the untreated group. Flow cytometry assay indicated that the cell cycles of the tumor cells were also altered by the compound. CONCLUSION Blue-Ⅰ could effectively suppress the gastric cancer cells proliferation. The mechanism perhaps involved in the apoptosis of gastric cancer cells induced by Blue-Ⅰ.
Key concepts: Apoptosis, Staining, Molecular biology, Comet assay, Cell growth, MTT assay, Flow cytometry, Cancer cell