Title of article :
Anti-cancer properties of Escherichia coli Nissle 1917 against HT- 29 colon cancer cells through regulation of Bax/Bcl-xL and AKT/ PTEN signaling pathways
Author/Authors :
Alizadeh, Siamak Department of Cell and Molecular Biology & Microbiology - Faculty of Biological Science and Technology - University of Isfahan, Isfahan , Esmaeili, Abolghasem Department of Cell and Molecular Biology & Microbiology - Faculty of Biological Science and Technology - University of Isfahan, Isfahan , Omidi, Yadollah Department of Pharmaceutics - Faculty of Pharmacy - Tabriz University of Medical Sciences, Tabriz
Pages :
8
From page :
886
To page :
893
Abstract :
Objective(s): Chemotherapies used to treat colon cancer might often fail due to the emergence of chemoresistance and side effects. Escherichia coli Nissle 1917 (EcN) is a beneficial probiotic, whose molecular mechanisms in the prevention of colon cancer are yet to be fully understood. The present study assessed the anti-cancer effects of EcN treatments in human colorectal cancer, HT-29 cell line, with the analysis of related mechanisms. Materials and Methods: The co-culture conditioned-media (CM) of EcN with adenocarcinoma HT- 29 cells and heat-inactivated bacteria (HIB) were applied for the treatment of the HT-29 cells. To study the inhibition potential of CM and HIB on cancer cells, various cellular/molecular analyses were implemented, including DAPI-staining and DNA ladder assays, flow cytometry and Real-time quantitative PCR (qPCR), as well as Western blotting analyses. Results: Our results indicated that EcN could elicit apoptotic impacts on the colon cancer HT-29 cells by up-regulating PTEN and Bax and down-regulating AKT1 and Bcl-xL genes. Conclusion: Based on our findings, EcN is proposed as a useful supplemental probiotic treatment against colon cancer.
Keywords :
AKT , Apoptosis , Cell signaling , Colon cancer , Escherichia coli Nissle1917
Journal title :
Iranian Journal of Basic Medical Sciences
Serial Year :
2020
Record number :
2516724
Link To Document :
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