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Cell cycle arrest and anti-cancer potential of probiotic Lactobacillus rhamnosus against HT-29 cancer cells

[Image: see text] Introduction: Nowadays, probiotic bacteria have been considered as a factor in the prevention and treatment of cancer, especially by induction of apoptosis. This study aimed to evaluate the cytotoxic, anti-proliferative, and apoptotic effects of the supernatant of probiotic Lactoba...

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Autores principales: Dehghani, Najme, Tafvizi, Farzaneh, Jafari, Parvaneh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Tabriz University of Medical Sciences (TUOMS Publishing Group) 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8494254/
https://www.ncbi.nlm.nih.gov/pubmed/34631486
http://dx.doi.org/10.34172/bi.2021.32
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author Dehghani, Najme
Tafvizi, Farzaneh
Jafari, Parvaneh
author_facet Dehghani, Najme
Tafvizi, Farzaneh
Jafari, Parvaneh
author_sort Dehghani, Najme
collection PubMed
description [Image: see text] Introduction: Nowadays, probiotic bacteria have been considered as a factor in the prevention and treatment of cancer, especially by induction of apoptosis. This study aimed to evaluate the cytotoxic, anti-proliferative, and apoptotic effects of the supernatant of probiotic Lactobacillus rhamnosus on HT-29 cell line. Methods : Molecular identification of probiotic L. rhamnosus was carried out using specific primers of 16S rRNA gene and sequencing. HT-29 cells were treated with different concentrations of bacterial supernatants at 24, 48, and 72 hours. MTT assay, Annexin V-FITC, real-time PCR, cell cycle analysis, and DAPI staining tests were conducted to evaluate the induction of apoptosis. The level of cyclin D1 protein was measured by immunocytochemistry method. Results: The supernatant of L. rhamnosus inhibited the growth of HT-29 cancer cells in a dose- and time-dependent manner. The results of flow cytometry confirmed apoptotic cell death. Probiotic bacterial supernatant caused up-regulation of pro-apoptotic genes including caspase-3, caspase-9, and Bax. In addition, they resulted in down-regulation of Bcl2 and a decrease in expression levels of cyclin D1, cyclin E, and ERBB2 genes. Cancer cells were arrested in the G0/G1 phase of the cell cycle. The results of immunocytochemistry showed significant down-regulation of cyclin D1 protein during the 48 hours treatment with bacterial supernatant compared to the untreated cells. Conclusion: The supernatant of probiotic L. rhamnosus has a great potential to inhibit the proliferation of HT-29 cells and the induction of apoptosis. L. rhamnosus might be used as a biological anti-cancer factor in the prevention and treatment of colon cancer.
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spelling pubmed-84942542021-10-08 Cell cycle arrest and anti-cancer potential of probiotic Lactobacillus rhamnosus against HT-29 cancer cells Dehghani, Najme Tafvizi, Farzaneh Jafari, Parvaneh Bioimpacts Original Research [Image: see text] Introduction: Nowadays, probiotic bacteria have been considered as a factor in the prevention and treatment of cancer, especially by induction of apoptosis. This study aimed to evaluate the cytotoxic, anti-proliferative, and apoptotic effects of the supernatant of probiotic Lactobacillus rhamnosus on HT-29 cell line. Methods : Molecular identification of probiotic L. rhamnosus was carried out using specific primers of 16S rRNA gene and sequencing. HT-29 cells were treated with different concentrations of bacterial supernatants at 24, 48, and 72 hours. MTT assay, Annexin V-FITC, real-time PCR, cell cycle analysis, and DAPI staining tests were conducted to evaluate the induction of apoptosis. The level of cyclin D1 protein was measured by immunocytochemistry method. Results: The supernatant of L. rhamnosus inhibited the growth of HT-29 cancer cells in a dose- and time-dependent manner. The results of flow cytometry confirmed apoptotic cell death. Probiotic bacterial supernatant caused up-regulation of pro-apoptotic genes including caspase-3, caspase-9, and Bax. In addition, they resulted in down-regulation of Bcl2 and a decrease in expression levels of cyclin D1, cyclin E, and ERBB2 genes. Cancer cells were arrested in the G0/G1 phase of the cell cycle. The results of immunocytochemistry showed significant down-regulation of cyclin D1 protein during the 48 hours treatment with bacterial supernatant compared to the untreated cells. Conclusion: The supernatant of probiotic L. rhamnosus has a great potential to inhibit the proliferation of HT-29 cells and the induction of apoptosis. L. rhamnosus might be used as a biological anti-cancer factor in the prevention and treatment of colon cancer. Tabriz University of Medical Sciences (TUOMS Publishing Group) 2021 2020-08-10 /pmc/articles/PMC8494254/ /pubmed/34631486 http://dx.doi.org/10.34172/bi.2021.32 Text en © 2021 The Author(s) https://creativecommons.org/licenses/by-nc/4.0/ This work is published by BioImpacts as an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ). Non-commercial uses of the work are permitted, provided the original work is properly cited.
spellingShingle Original Research
Dehghani, Najme
Tafvizi, Farzaneh
Jafari, Parvaneh
Cell cycle arrest and anti-cancer potential of probiotic Lactobacillus rhamnosus against HT-29 cancer cells
title Cell cycle arrest and anti-cancer potential of probiotic Lactobacillus rhamnosus against HT-29 cancer cells
title_full Cell cycle arrest and anti-cancer potential of probiotic Lactobacillus rhamnosus against HT-29 cancer cells
title_fullStr Cell cycle arrest and anti-cancer potential of probiotic Lactobacillus rhamnosus against HT-29 cancer cells
title_full_unstemmed Cell cycle arrest and anti-cancer potential of probiotic Lactobacillus rhamnosus against HT-29 cancer cells
title_short Cell cycle arrest and anti-cancer potential of probiotic Lactobacillus rhamnosus against HT-29 cancer cells
title_sort cell cycle arrest and anti-cancer potential of probiotic lactobacillus rhamnosus against ht-29 cancer cells
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8494254/
https://www.ncbi.nlm.nih.gov/pubmed/34631486
http://dx.doi.org/10.34172/bi.2021.32
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