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2014 ; 5
(5
): 675-80
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
The bacterial genotoxin colibactin promotes colon tumor growth by modifying the
tumor microenvironment
#MMPMID25483338
Dalmasso G
; Cougnoux A
; Delmas J
; Darfeuille-Michaud A
; Bonnet R
Gut Microbes
2014[]; 5
(5
): 675-80
PMID25483338
show ga
The gut microbiota is suspected to promote colorectal cancer (CRC). Escherichia
coli are more frequently found in CCR biopsies than in healthy mucosa;
furthermore, the majority of mucosa-associated E. coli isolated from CCR harbors
the pks genomic island (pks+ E. coli) that is responsible for the synthesis of
colibactin, a genotoxic compound. We have recently reported that transient
contact of a few malignant cells with colibactin-producing E. coli increases
tumor growth in a xenograft mouse model. Growth is sustained by cellular
senescence that is accompanied by the production of growth factors. We
demonstrated that cellular senescence is a consequence of the pks+ E.
coli-induced alteration of p53 SUMOylation, an essential post-translational
modification in eukaryotic cells. The underlying mechanisms for this process
involve the induction of miR-20a-5p expression, which targets SENP1, a key
protein in the regulation of the SUMOylation process. These results are
consistent with the expression of SENP1, miR-20a-5p and growth factors that are
observed in a CRC mouse model and in human CCR biopsies colonized by pks+ E.
coli. Overall, the data reveal a new paradigm for carcinogenesis in which pks+ E.
coli infection induces cellular senescence characterized by the production of
growth factors that promote the proliferation of uninfected cells and,
subsequently, tumor growth.
|Animals
[MESH]
|Colonic Neoplasms/*pathology
[MESH]
|Cysteine Endopeptidases
[MESH]
|Endopeptidases/metabolism
[MESH]
|Escherichia coli/genetics/*growth & development
[MESH]
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free
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