Gut bacteria promote proliferation in benign S/RG/C2 colorectal tumour cells, and promote proliferation, migration and invasion in malignant HCT116 cells.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
12 10 2023
Historique:
received: 15 03 2023
accepted: 04 10 2023
medline: 2 11 2023
pubmed: 13 10 2023
entrez: 12 10 2023
Statut: epublish

Résumé

Colorectal cancer (CRC) is a significant global health burden with a rising incidence worldwide. Distinct bacterial populations are associated with CRC development and progression, and it is thought that the relationship between CRC and associated gut bacteria changes during the progression from normal epithelium to benign adenoma and eventually malignant carcinoma and metastasis. This study compared the interaction of CRC-associated species Enterotoxigenic Bacteroides fragilis, Enterococcus faecalis and Fusobacterium nucleatum and one probiotic species, Escherichia coli Nissle 1917 with a colorectal adenoma (S/RG/C2) and a colorectal adenocarcinoma (HCT116) derived cell line. Gentamicin protection assays showed that all species displayed higher attachment to benign tumour monolayers when compared to malignant monolayers. However, invasion of 3/4 species was higher in the HCT116 cells than in the adenoma cells. All species were found to persist within tumour cell monolayers for a minimum of 48 h under standard aerobic cell culture conditions, with persistence significantly higher in HCT116 cells. Downstream assays were performed to analyse the behaviour of S/RG/C2 and HCT116 cells post-infection and revealed that all species increased the tumour cell yield of both cell lines. The migratory and invasive potential of HCT116 cells was increased after infection with F. nucleatum; however, no species significantly altered these characteristics in S/RG/C2 cells. These results add to the growing evidence for the involvement of microorganisms in CRC progression and suggest that these interactions may be dependent on tumour cell-specific characteristics.

Identifiants

pubmed: 37828235
doi: 10.1038/s41598-023-44130-6
pii: 10.1038/s41598-023-44130-6
pmc: PMC10570319
doi:

Banques de données

figshare
['10.6084/m9.figshare.21310797']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

17291

Informations de copyright

© 2023. Springer Nature Limited.

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Auteurs

J L Robson (JL)

Department of Applied Sciences, University of the West of England, Bristol, England.

R M S Thorn (RMS)

Department of Applied Sciences, University of the West of England, Bristol, England.

A C Williams (AC)

School of Cellular and Molecular Medicine, University of Bristol, Bristol, England.

T J Collard (TJ)

School of Cellular and Molecular Medicine, University of Bristol, Bristol, England.

D Qualtrough (D)

Department of Applied Sciences, University of the West of England, Bristol, England. David.Qualtrough@uwe.ac.uk.

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