The effect of intestinal microbiota metabolites on HT29 cell line using MTT method in patients with colorectal cancer.

Cell line Colorectal cancer MTT Metabolites

Journal

Gastroenterology and hepatology from bed to bench
ISSN: 2008-2258
Titre abrégé: Gastroenterol Hepatol Bed Bench
Pays: Iran
ID NLM: 101525875

Informations de publication

Date de publication:
2019
Historique:
entrez: 27 2 2020
pubmed: 27 2 2020
medline: 27 2 2020
Statut: ppublish

Résumé

The aim of this study was to evaluate the effect of intestinal microbiota metabolites in colorectal cancer patients on HT29 cell line using MTT assay. Colorectal cancer is one of the most common malignant tumors. Human guts harbor abundant microbes that adjust many aspects of the host physiology. Increasing studies suggest that gut microbiota play a significant role in the incidence and expansion of CRC, as a result of virulence factors, bacterial metabolites, or inflammatory pathways. In this cross-sectional study, 60 biopsy samples including 30 cancerous and 30 adjacent healthy tissues were collected from patients with CRC during 2017. Biopsy samples were first cultured on Thioglycollate broth medium for 24hr after which the microbiota metabolites were filtered and stored at -20 C° for further evaluation. HT29 cells were treated by microbiota metabolites at different times (3, 6, 12, 18h) and its viability was assessed by MTT assay. The cells treated with microbiota metabolites showed increased viability and proliferation in time-dependent analysis by MTT assay, but there was not significant differences between the two groups. It seems that microbial metabolites are able to induce proliferation and increase cell viability and thus induce colorectal cancer.

Sections du résumé

AIM OBJECTIVE
The aim of this study was to evaluate the effect of intestinal microbiota metabolites in colorectal cancer patients on HT29 cell line using MTT assay.
BACKGROUND BACKGROUND
Colorectal cancer is one of the most common malignant tumors. Human guts harbor abundant microbes that adjust many aspects of the host physiology. Increasing studies suggest that gut microbiota play a significant role in the incidence and expansion of CRC, as a result of virulence factors, bacterial metabolites, or inflammatory pathways.
METHODS METHODS
In this cross-sectional study, 60 biopsy samples including 30 cancerous and 30 adjacent healthy tissues were collected from patients with CRC during 2017. Biopsy samples were first cultured on Thioglycollate broth medium for 24hr after which the microbiota metabolites were filtered and stored at -20 C° for further evaluation. HT29 cells were treated by microbiota metabolites at different times (3, 6, 12, 18h) and its viability was assessed by MTT assay.
RESULTS RESULTS
The cells treated with microbiota metabolites showed increased viability and proliferation in time-dependent analysis by MTT assay, but there was not significant differences between the two groups.
CONCLUSION CONCLUSIONS
It seems that microbial metabolites are able to induce proliferation and increase cell viability and thus induce colorectal cancer.

Identifiants

pubmed: 32099605
pmc: PMC7011068

Types de publication

Journal Article

Langues

eng

Pagination

S74-S79

Informations de copyright

©2019 RIGLD.

Déclaration de conflit d'intérêts

The authors declare that they have no conflict of interest.

Références

PLoS One. 2016 May 19;11(5):e0155772
pubmed: 27196402
Arch Pharm Res. 2001 Dec;24(6):564-7
pubmed: 11794536
Nat Rev Endocrinol. 2016 Mar;12(3):133-43
pubmed: 26678807
Cancers (Basel). 2019 Jan 03;11(1):
pubmed: 30609850
World J Gastroenterol. 2013;19(43):7531-43
pubmed: 24431894
Sci Transl Med. 2012 Jun 6;4(137):137rv7
pubmed: 22674557
Biosens Bioelectron. 2004 Nov 1;20(4):699-705
pubmed: 15522584
PLoS One. 2012;7(5):e36957
pubmed: 22606315
Carcinogenesis. 1997 Dec;18(12):2353-9
pubmed: 9450481
Roum Arch Microbiol Immunol. 2011 Jul-Sep;70(3):134-40
pubmed: 22570928
Gastroenterol Hepatol Bed Bench. 2019 Fall;12(4):358-363
pubmed: 31749925
Gastroenterol Hepatol Bed Bench. 2019 Spring;12(2):149-154
pubmed: 31191840
Int J Mol Sci. 2018 Mar 03;19(3):
pubmed: 29510500
Gastroenterol Hepatol Bed Bench. 2018 Spring;11(2):101-109
pubmed: 29910850
Cancer Lett. 2006 Aug 18;240(1):143-7
pubmed: 16288832
FEMS Microbiol Ecol. 2008 Dec;66(3):487-95
pubmed: 18537837
Biologics. 2011;5:71-86
pubmed: 21847343
Cancer Cell. 2018 Jun 11;33(6):954-964
pubmed: 29657127
Regul Toxicol Pharmacol. 2004 Dec;40(3):319-26
pubmed: 15546686
PLoS One. 2011;6(5):e20447
pubmed: 21647227
J Lipid Res. 2006 Feb;47(2):241-59
pubmed: 16299351
Nat Microbiol. 2017 Feb 22;2:17008
pubmed: 28225000
Anim Nutr. 2016 Jun;2(2):99-104
pubmed: 29767022
Cancer J. 2014 May-Jun;20(3):181-9
pubmed: 24855005
PLoS One. 2009 Jun 24;4(6):e6026
pubmed: 19551144

Auteurs

Somayeh Jahani-Sherafat (S)

Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Masoumeh Azimirad (M)

Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Hajieh Ghasemian-Safaei (H)

Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Hadi Ahmadi Amoli (H)

Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Sharareh Moghim (S)

Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Ghazal Sherkat (G)

Student Research Committee, Islamic Azad University, Mashhad Branch, Mashhad, Iran.

Mohammad Reza Zali (MR)

Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Classifications MeSH