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Original Article
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| Anisomycin represses in vitro and in vivo colon adenocarcinoma CT26 cell growth via activation of caspase-cascade with reduction of carcinoembryonic antigen | ||||||
| Pengtao You1, Haifeng Fu1, Zhiwei Zhou1, Yuan Wang1, Manman Sun1, Jing Liu2, Feiyue Xing1 | ||||||
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1Department of Immunobiology, Institute of Tissue Transplantation and Immunology, Jinan University, Guangzhou, P. R. China.
2Department of Stomatology, Jinan University, Guangzhou, P. R. China. | ||||||
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| You P, Fu H, Zhou Z, Wang Y, Sun M, Liu J, Xing F. Anisomycin represses in vitro and in vivo colon adenocarcinoma CT26 cell growth via activation of caspase-cascade with reduction of carcinoembryonic antigen. Edorium J Biomolecules 2015;1:1–9. |
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Abstract
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Aims:
In vitro evidence indicates that anisomycin can induce cell apoptosis. This study was to evaluate potential of anisomycin to treat colon adenocarcinoma in vitro and in vivo.
Methods: Cell viability was determined by methyl thiazolyl-tetrazolium bromide (MTT). Cell cycle and apoptosis were detected by flow cytometry. CT26 colon adenocarcinoma model was established. Cellular apoptosis and tumor necrosis were detected by TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling), and H&E staining. Carcinoembryonic antigen (CEA) was detected by in situ immunofluorescence. Expressions of caspases were measured by Western Blot. Results: Our results showed that multipoint intratumoral administration of anisomycin significantly suppressed colon adenocarcinoma CT26 cell growth, and resulted in the survival of approximately 80% of CT26-bearing mice 50 days after CT26 inoculation, superior dramatically to adriamycin. Anisomycin inhibited the proliferation of CT26 cells, and arrested the cells into S and G2/M phases with the production of sub-diploid cells. Anisomycin induced in vitro and in vivo apoptosis of CT26 cells, which was consistent with the enhanced expressions of caspases. Specially, the apoptotic rate of the tumor cells in the anisomycin-treated mice was higher than that in the adriamycin-treated mice, which was supported by the observed histopathological and immunochemical changes in the tumor tissue. Carcinoembryonic antigen-positive cells in the tumor tissues also were prominently decreased by anisomycin. Conclusion: These results indicate first time that anisomycin efficaciously represses growth of colon adenocarcinoma with the extended survival through activation of caspase signaling with reduction of CEA, significantly superior to adriamycin. Thus, it is a promising drug to be applied to colon adenocarcinoma therapy. | |
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Keywords:
Anisomycin, Apoptosis, Carcinoembryonic antigen, Colon adenocarcinoma
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Author Contributions:
Pengtao You – Acquisition of data, Analysis and interpretation of data, Drafting the article, Final approval of the version to be published Haifeng Fu – Acquisition of data, Analysis and interpretation of data, Revising it critically for important intellectual content, Final approval of the version to be published Zhiwei Zhou – Acquisition of data, Revising it critically for important intellectual content, Final approval of the version to be published Yuan Wang – Acquisition of data, Revising it critically for important intellectual content, Final approval of the version to be published Manman Sun – Acquisition of data, Revising it critically for important intellectual content, Final approval of the version to be published Jing Liu – Substantial contributions to conception and design, Analysis and interpretation of data, Revising it critically for important intellectual content, Final approval of the version to be published Feiyue Xing – Substantial contributions to conception and design, Analysis and interpretation of data, Drafting the article, Revising it critically for important intellectual content, Final approval of the version to be published |
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Guarantor of submission
The corresponding author is the guarantor of submission. |
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Source of support
None |
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Conflict of interest
Authors declare no conflict of interest. |
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Copyright
© 2015 Pengtao You et al. This article is distributed under the terms of Creative Commons Attribution License which permits unrestricted use, distribution and reproduction in any medium provided the original author(s) and original publisher are properly credited. Please see the copyright policy on the journal website for more information. |
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