The bacterial genotoxin colibactin promotes colon tumor growth by modifying the tumor microenvironment
Open accessAbstract
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.
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TL;DR
Colibactin-producing *E. coli* (pks+ *E. coli*) induce cellular senescence in intestinal epithelial cells via a c-Myc/miR-20a-5p/SENP1 axis that increases SUMO-conjugated p53, and the resulting senescence-associated secretory phenotype (notably HGF) promotes proliferation of uninfected cells and tumor growth. The authors propose that pks+ *E. coli* modify the tumor microenvironment to favor colon tumor promotion.
Key findings
- Transient infection of HCT116 xenografts in nude mice at low MOI (20) increased tumor growth and Ki67-positive cells, whereas high MOI (100) decreased tumor growth, consistent with tumor dormancy from massive cell-cycle arrest (n = 5/group; *P* < 0.05).
- Conditioned medium from pks+ *E. coli*-infected cells increased proliferation of uninfected cells to a degree similar to medium with 10% fetal bovine serum; this was reproduced across Int-407, HCT8, Caco-2, HT-29, HCT116 and non-transformed IEC-6 cells.
- pks+ *E. coli* induced senescence (SA-β-gal, phospho-p53, p21^Cip, Rb accumulation, decreased E2F-1) with increased HGF, FGF and GM-CSF; tumors at day 10 post-implantation showed an ~3-fold increase in the percentage of senescent cells versus pks− controls.
- An HGF pathway inhibitor (and neutralizing antibodies) abrogated the pro-proliferative activity of conditioned medium and significantly blocked xenograft growth; mechanistically, pks+ *E. coli* induced c-Myc, which drove miR-20a-5p, which bound the SENP1 3′-UTR and reduced SENP1, increasing SUMO1-conjugated p53.
- In the AOM/DSS model, colonization with a clinical pks+ *E. coli* strain significantly increased colon tumor number versus the isogenic pks mutant, without affecting inflammatory score or tumor size; γH2Ax, miR-20a-5p, SA-β-gal, p21^Cip and HGF pathway activation were increased. Human colon adenocarcinoma biopsies colonized by pks+ *E. coli* showed the same signature (high γH2Ax, miR-20a-5p, senescence markers, HGF mRNA and activated HGF receptors; decreased SENP1-expressing cells), differentiating them from pks−-colonized tumors by redundancy analyses.
Methods
- Xenograft model: HCT116 cells (2 × 10⁶) subcutaneously injected into nude mice and infected for 3 hours with pks+ *E. coli* or isogenic pks− *E. coli* at MOI 20 or 100; tumor size monitored over time.
- In vitro assays: conditioned medium transfer to measure proliferation of uninfected cells across multiple intestinal epithelial lines; SA-β-gal, senescence protein profiles, growth factor expression, SUMOylation patterns, miR-20a-5p/SENP1 reporter and transfection experiments, and inhibitor/neutralizing antibody treatments.
- In vivo validation: AOM/DSS (azoxymethane/dextran sodium sulfate) CRC mouse model colonized with a clinical pks+ *E. coli* strain versus its isogenic pks mutant, plus analysis of human colon adenocarcinoma biopsies colonized by pks+ versus pks− *E. coli* (including redundancy analyses).
Limitations
- Stated: pks+ *E. coli*-induced senescence was also observed in p53−/− cells, suggesting pathways other than p53 signaling may be involved.
- Stated: no increase in tumor size was observed with pks+ *E. coli* in the AOM/DSS model in immunocompetent mice, possibly because senescent tumors generate an immune response that constrains expansion; the authors note the promoting effect on intestinal tumor size may be difficult to observe.
- Stated: the study focused on colibactin as the sole toxin affecting the cell cycle, but clinical pks+ *E. coli* frequently also produce CNF1, whose impact on CRC remains to be explored; overall understanding of the cancer-promoting potential of pks+ *E. coli* remains limited and clinical consequences need clarification.
- Evident from the text: several supporting results are described as "unpublished data" (e.g., high-MOI growth decrease, SUMOylation patterns, anacardic acid and SENP1 overexpression effects), and the role of the dormancy-type interaction in intestinal tumors "remains to be assessed."
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- Findingown data
miR-20a-5p binds to the SENP1 mRNA 3'-UTR.
“In addition, using a reporter assay, we demonstrated that miR-20a-5p binds to the SENP1 mRNA 3'-UTR.”
Quote in the paperSubstantial claim - Findingown data
pksC E. coli-infected cells displayed a modified pattern of SUMO-conjugated proteins compared with pks-E. coli-infected cells or uninfected cells.
“pksC E. coli-infected cells displayed a modified pattern of SUMO-conjugated proteins compared with pks-E.coliinfected cells or uninfected cells (unpublished data).”
Quote in the paperSubstantial claim - Findingown data
pksC E. coli, unlike pks-E. coli, induced a time-dependent and dose-dependent increase in SA-b-gal activity in infected cells.
“pksC E. coli, in contrast to pks-E.coli, induced a time- dependent and dose-dependent increase in SA-b-gal activity.”
Quote in the paperSubstantial claim - Findingown data
Expression levels of FGF, GM-CSF, and HGF were increased in xenografts at 10 days post-pksC E. coli infection compared to xenografts infected with pks-E. coli.
“Of note, the expression levels of FGF, GM-CSF and HGF were also increased in xenografts at 10 d post-pksC E. coli infection compared to xenografts infected with pks-E.coli.”
Quote in the paperSubstantial claim- Rests on an assumption: The subcutaneous xenograft model in immunodeficient mice is a valid model for the effect of pksC E. coli on human colon tumor growth.
- Findingown data
pksC E. coli-infected cells expressed significantly higher levels of HGF, FGF, and GM-CSF than pks-E. coli-infected cells.
“Interestingly, pksC E. coli-infected cells expressed significantly higher levels of the growth factors HGF, FGF, and GM-CSF than pks-E.coli-infected cells.”
Quote in the paperSubstantial claim
- Findingown data
Transfection of cells with mature miR-20a-5p decreased SENP1 expression at both the mRNA and protein levels.
“Furthermore, transfection of cells with mature miR-20a-5p decreased SENP1 expression at both the mRNA and protein levels.”
Quote in the paperSubstantial claim - Findingown data
Over-expression of functional SENP1, unlike over-expression of an inactive SENP1, significantly decreased the number of senescent cells induced by pksC E. coli infection.
“Interestingly, over-expression of SENP1, unlike overexpression of an inactive SENP1, significantly decreased the number of senescent cells induced by pksC E. coli infection, confirming the role of SENP1 in pksC E. coli-induced senescence.”
Quote in the paperSubstantial claim - Findingown data
In intestinal epithelial cell xenografts in nude mice, a single and transient exposure to pksC E. coli at MOI 20 was associated with increased tumor growth and Ki67-positive cell numbers.
“In this model, a single and transient exposure of xenografts to pksC E. coli at a multiplicity of infection (MOI) of 20 was associated with an increase in tumor growth and Ki67positive cell numbers, suggesting that pksC E. coli enhance cell proliferation (Fig. 1A).”
Quote in the paperSubstantial claim- Rests on an assumption: The subcutaneous xenograft model in immunodeficient mice is a valid model for the effect of pksC E. coli on human colon tumor growth.
- Findingown data
An HGF pathway inhibitor abrogated the pro-proliferative activity of conditioned medium from pksC E. coli-infected cells in vitro.
“An HGF pathway inhibitor, in contrast to vehicle or other growth factor inhibitors abrogated the pro-proliferative activity of CM in vitro.”
Quote in the paperSubstantial claim - Findingown data
An anti-miR-20a-5p abrogated pksC E. coli-induced accumulation of SUMO1-conjugated p53 and cellular senescence.
“Furthermore, an anti-miR-20a-5p abrogated pksC E. coli-induced accumulation of SUMO1-conjugated p53 and, consequently, cellular senescence.”
Quote in the paperSubstantial claim - Findingown data
In cells transfected with miR-20a-5p, a significant increase in the number of senescent cells was observed compared to cells transfected with a miR-control.
“In cells transfected with miR-20a-5p, a significant increase in the number of senescent cells was observed compared to cells transfected with a miRcontrol.”
Quote in the paperSubstantial claim - Findingown data
A clinical pksC E. coli strain induced tumor activation of the HGF pathway, characterized by high levels of HGF mRNA and phosphorylation of HGF receptors.
“Finally, a clinical pksC E. coli strain induced tumor activation of the HGF pathway, which was characterized by high levels of HGF mRNA and phosphorylation of HGF receptors.”
Quote in the paperSubstantial claim- Rests on an assumption: The AOM/DSS mouse model is a valid model for human colorectal cancer promotion by pksC E. coli.
- Findingown data
The pro-proliferative effect of conditioned medium from pksC E. coli-infected cells was observed using various intestinal epithelial cell lines and non-transformed IEC-6 cells.
“Similar results were obtained using various intestinal epithelial cells lines (Int-407, HCT8, Caco-2, HT-29 and HCT116) and non-transformed IEC-6 cells.”
Quote in the paperSubstantial claim - Findingown data
pksC E. coli-induced senescence was also observed in p53 -/- cells.
“However, it should be noted that pksC E. coliinduced senescence was also observed in p53 -/-cells, suggesting that pathways other than p53 signaling could be involved in the senescence process.”
Quote in the paperSubstantial claim - Findingreasoning
Xenografts infected by pksC E. coli at a high MOI of 100 showed decreased tumor growth.
“xenografts infected by pksC E. coli at a high MOI (i.e.100) resulted in a decrease in tumor growth (unpublished data, Fig. 1A).”
Quote in the paperNot a substantial claim- Rests on an assumption: The subcutaneous xenograft model in immunodeficient mice is a valid model for the effect of pksC E. coli on human colon tumor growth.
- Findingown data
miR-20a-5p expression was significantly up-regulated in pksC E. coli-infected cells, unlike in pks-E. coli-infected cells.
“Interestingly, miR-20a-5p expression was significantly up-regulated in pksC E. coliinfected cells, unlike in pks-E.coliinfected cells.”
Quote in the paperSubstantial claim - Findingown data
At day 10 post-implantation, tumors derived from pksC E. coli-infected cells exhibited an approximately 3-fold increase in the percentage of senescent cells compared to tumors derived from pks-E. coli-infected cells.
“Although tumor sizes were comparable at this early time, tumors derived from pksC E. coli-infected cells exhibited an »3-fold increase in the percentage of senescent cells compared to tumors derived from pks-E.coli-infected cells.”
Quote in the paperSubstantial claim- Rests on an assumption: The subcutaneous xenograft model in immunodeficient mice is a valid model for the effect of pksC E. coli on human colon tumor growth.
- Findingown data
Anti-miR-20a-5p abolished the effect of pksC E. coli on HGF expression and cell proliferation.
“In contrast, anti-miR-20a-5p abolished the effect of pksC E. coli on HGF expression and cell proliferation.”
Quote in the paperSubstantial claim - Findingown data
Colonization of AOM/DSS-treated mice with a clinical pksC E. coli strain significantly increased the number of colon tumors compared to mice infected with the isogenic pks mutant.
“The colonization of AOM/DSS-treated mice gut significantly increased the number of colon tumors in comparison to mice infected with the clinical strain mutated in the pks island (isogenic mutant).”
Quote in the paperSubstantial claim- Rests on an assumption: The AOM/DSS mouse model is a valid model for human colorectal cancer promotion by pksC E. coli.
- Findingown data
Conditioned medium derived from pksC E. coli-infected cells over-expressing a functional SENP1 did not promote cell proliferation.
“Of note, CM derived from pksC E. coli-infected cells over-expressing a functional SENP1 did not promote cell proliferation.”
Quote in the paperSubstantial claim - Findingown data
Anacardic acid, an inhibitor of protein SUMOylation, abrogated pksC E. coli-induced senescence.
“Furthermore, the use of anacardic acid, an inhibitor of protein SUMOylation, 16 abrogated pksC E. coliinduced senescence (unpublished data).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [16] source
Not checked in the free run.
- Findingown data
Conditioned medium derived from pksC E. coli-infected intestinal epithelial cells increased the proliferation of uninfected cells.
“Only CM derived from pksC E. coli-infected cells increased the proliferation of uninfected cells, and the enhancement was similar to that obtained with medium containing 10% fetal bovine serum.”
Quote in the paperSubstantial claim - Findingown data
HGF inhibitor significantly blocked the growth of xenografts obtained from cells infected with pksC E. coli.
“As observed in vitro, HGF inhibitor significantly blocked the growth of xenografts obtained from cells infected with pksC E. coli.”
Quote in the paperSubstantial claim- Rests on an assumption: The subcutaneous xenograft model in immunodeficient mice is a valid model for the effect of pksC E. coli on human colon tumor growth.
- Findingown data
In the AOM/DSS colon cancer model using immunocompetent mice, no increase in tumor size was observed in response to pksC E. coli infection.
“However, we did not observe an increase in tumor size in response to pksC E. coli infection in the AOM/DSS colon cancer model using immunocompetent mice.”
Quote in the paperSubstantial claim- Rests on an assumption: The AOM/DSS mouse model is a valid model for human colorectal cancer promotion by pksC E. coli.
- Findingown data
These biological stigmas significantly differentiated human CCR colonized by pksC E. coli from those colonized by pks-E. coli, as shown by redundancy analyses.
“These biological stigmas significantly differentiated human CCR colonized by pksC E. coli from those colonized by pks-E.coli, as shown by redundancy analyses.”
Quote in the paperSubstantial claim - Findingnone given
In the AOM/DSS murine colon cancer model, the neoplastic grade tended to increase after 7 weeks of colonization by pksC E. coli.
“Similarly, in the AOM/DSS murine colon cancer model, the neoplastic grade tended to increase after 7 weeks of colonization by pksC E. coli.”
Quote in the paperSubstantial claim- Rests on an assumption: The AOM/DSS mouse model is a valid model for human colorectal cancer promotion by pksC E. coli.
- Interpretationcitation
pksC E. coli may support a permissive, senescent microenvironment that promotes tumourigenesis by inducing the production of growth factors that fuel uninfected tumor cells.
“pksC E. coli may thereby support a permissive, senescent microenvironment that has been reported to relax the control over cell behavior 21 and promote tumourigenesis by inducing the production of growth factors that fuel the uninfected tumor cells (Fig. 1C).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [21] source
Not checked in the free run.
- Interpretationreasoning
pksC E. coli may also support a permissive microenvironment that favors cancer cell invasion and aggressiveness.
“pksC E. coli may therefore also support a permissive microenvironment that favors cancer cell invasion and aggressiveness.”
Quote in the paperSubstantial claim - Interpretationown data
pksC E. coli induce senescence by subverting the SUMOylation process via SENP1 downregulation under the control of a miRNA.
“They also induce senescence by subverting the SUMOylation process via SENP1 downregulation under the control of a miRNA.”
Quote in the paperSubstantial claim - Interpretationown data
Our data support the hypothesis that colibactin-producing bacteria can play an important role in colorectal cancer.
“In conclusion, our data support the hypothesis that colibactin-producing bacteria can play an important role in CRC.”
Quote in the paperSubstantial claim - Interpretationown data
Overall, the data indicate that pksC E. coli impact the physiopathology of colorectal cancer.
“Overall, these data indicate that pksC E. coli impact the physiopathology of CRC.”
Quote in the paperSubstantial claim
- May combine two claims. 12
May combine two claims.
Findingown datapksC E. coli did not affect the inflammatory score or the size of tumors in the AOM/DSS model.
“pksC E. coli did not affect the inflammatory score or the size of the tumors.”
Quote in the paperNot a substantial claim- Rests on an assumption: The AOM/DSS mouse model is a valid model for human colorectal cancer promotion by pksC E. coli.
May combine two claims.
FindingcitationpksC E. coli-infected cells exhibited accumulation of phospho-p53, p21 Cip, and Retinoblastoma protein and decreased E2F-1 expression at day 5 post-infection.
“pksC E. coli-infected cells exhibited an accumulation of phospho-p53, p21 Cip , and Retinoblastoma protein as well as a decrease in E2F-1 expression at day 5 post-infection, which correspond to a protein expression profile characteristic of senescent cells.12”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [12] source
Not checked in the free run.
May combine two claims.
Findingown dataCells transfected with miR-20a-5p produced significant levels of HGF, and their conditioned medium induced the proliferation of untransfected cells.
“As observed upon pksC E. coli infection, cells transfected with miR-20a-5p produced significant levels of HGF, and their CM induced the proliferation of untransfected cells.”
Quote in the paperSubstantial claimMay combine two claims.
FindingcitationpksC E. coli infection caused accumulation of SUMO1-conjugated p53 and was associated with a decrease in SENP1 expression.
“Accordingly, we observed an accumulation of SUMO1-conjugated p53, which is known to drive cellular senescence.17 This accumulation was associated with a decrease in SENP1 expression, a key enzyme involved in the control of the SUMOylation process.17”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [17] source
Not checked in the free run.
May combine two claims.
Findingown datapksC E. coli infection induced c-Myc expression and its binding to the miR-20a-5p promoter.
“Accordingly, we observed that pksC E. coli infection, which is known to induce DNA damage, 9,10 induced c-Myc expression and its binding to the miR-20a-5p promoter.”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
Findingown dataTime-course experiments showed that pksC E. coli induced c-Myc expression 3 days after infection, followed by modifications of miR-20a-5p and SENP1 expression levels 2 days later.
“Finally, time-course experiments showed that pksC E. coli induced c-Myc expression 3 d after infection, followed by modifications of miR-20a-5p and SENP1 expression levels 2 d later.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataTransfection of pksC E. coli-infected cells with c-Myc siRNA reduced miR-20a-5p expression, increased SENP1 expression, reduced SUMO-conjugated p53, decreased senescent cells, and abolished the pro-proliferative effect of conditioned medium.
“Transfection of pksC E. coli-infected cells with c-Myc siRNA strongly reduced the expression of miR20a-5p, increased the expression of SENP1, reduced the level of SUMO-conjugated p53, decreased the number of pksC E. coli-induced senescent cells and consequently abolished the pro-proliferative effect of the CM derived from those cells.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataThe DNA damage marker gH2Ax, miR-20a-5p expression, and senescence markers were significantly increased in tumors from mice colonized by clinical pksC E. coli compared with those from mice colonized by the isogenic mutant.
“The DNA damage marker gH2Ax, the miR-20a-5p expression level and senescence markers (SA-b-gal activity and p21 cip expression) were significantly increased in tumors isolated from mice colonized by the clinical pksC E. coli strain compared with those isolated from mice colonized by the corresponding isogenic mutant.”
Quote in the paperSubstantial claim- Rests on an assumption: The AOM/DSS mouse model is a valid model for human colorectal cancer promotion by pksC E. coli.
May combine two claims.
Findingown dataHuman biopsies colonized by pksC E. coli harbored high expression levels of gH2Ax, miR-20a-5p, senescence markers, HGF mRNA, activated HGF receptors, and a decrease in the number of SENP1-expressing cells.
“As observed in the AOM/DSS mouse model, human biopsies colonized by pksC E. coli harbored high expression levels of gH2Ax, miR-20a-5p, senescence markers (SA-b-gal, p21 cip ), and HGF mRNA and activated HGF receptors, as well as a decrease in the number of SENP1-expressing cells.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown datapksC E. coli activate the miR-20a-5p/SENP1/senescence/HGF pathway in human and murine colon adenocarcinomas and therefore may contribute to colorectal cancer development.
“pksC E. coli activate the miR-20a-5p/SENP1/senescence/HGF pathway (Fig. 1B) in human and murine colon adenocarcinomas and therefore may contribute to CCR development.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataColibactin-producing E. coli modulate the tumor microenvironment by inducing the secretion of several growth factors from senescent cells, which can promote tumor growth.
“Our findings suggest that colibactin-producing E. coli modulate the tumor microenvironment by inducing the secretion of several growth factors from senescent cells, which can promote tumor growth.”
Quote in the paperSubstantial claim- Rests on an assumption: The subcutaneous xenograft model in immunodeficient mice is a valid model for the effect of pksC E. coli on human colon tumor growth.
May combine two claims.
InterpretationreasoningColibactin-producing bacteria can modulate the tumor microenvironment to favor the emergence of senescent cells, which may affect tumor promotion and cancer progression via the secretion of growth factors.
“Consequently, colibactinproducing bacteria can modulate the tumor microenvironment to favor the emergence of senescent cells, which may also affects tumor promotion and cancer progression via the secretion of growth factors.”
Quote in the paperSubstantial claim
The paper relies on this without support.
The pks genomic island is responsible for the synthesis of colibactin, a genotoxic compound.
“the majority of mucosa-associated E. coli isolated from CCR harbors the pks genomic island (pksC E. coli) that is responsible for the synthesis of colibactin, a genotoxic compound.”
The paper relies on this without support.
The subcutaneous xenograft model in immunodeficient mice is a valid model for the effect of pksC E. coli on human colon tumor growth.
“The promotion of tumor growth was clearly observed in the subcutaneous xenograft model using immunodeficient mice.”
The paper relies on this without support.
The AOM/DSS mouse model is a valid model for human colorectal cancer promotion by pksC E. coli.
“To confirm the reliability of our findings, we explored the impact of a clinical pksC E. coli strain in an AOM/DSS (azoxymethane/dextran sodium sulfate) CRC mouse model.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In several mouse models, other colibactin-producing E. coli have been observed to promote the development of colorectal cancer.
“in several mouse models, other colibactin-producing E. coli have been observed to promote the development of colorectal cancer [125–131]”
From Selection, Comparative Genomics, and Potential Probiotic Features of Escherichia coli 5C, a pks-Negative Strain Isolated from Healthy Infant Donor Feces (2026) · cites this paper as [129]
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Microbial Colonization Coordinates the Pathogenesis of a Klebsiella pneumoniae Infant Isolate
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Our Little Friends with Big Roles: Alterations of the Gut Microbiota in Thyroid Disorders
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ClbR Is the Key Transcriptional Activator of Colibactin Gene Expression in Escherichia coli
Wallenstein, A., Rehm, N., Brinkmann, M., Selle, M., Bossuet‐Greif, N., Sauer, D., Bunk, B., Spröer, C., Wami, H. T., Homburg, S., et al. (2020) · mSphere · doi:10.1128/msphere.00591-20 · Cited by 40 · see citing works
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Greathouse, K. L., & Choudhury, A. (2025) · Cell Host & Microbe · doi:10.1016/j.chom.2025.05.011 · Cited by 38 · see citing works
Molecular crosstalk between polyphenols and gut microbiota in cancer prevention
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- Authors
- Dalmasso, G., Cougnoux, A., Delmas, J., Darfeuille-Michaud, A., & Bonnet, R.
- Affiliations
- Inserm (FR)
- Corresponding author
- Bonnet, Richard
- Venue
- Gut Microbes
- Publisher
- Informa UK Limited
- Published
- 2014-09-03
- Volume
- 5
- Issue
- 5
- Pages
- 675-680
- ISSN
- 1949-0976 (ISSN-L)
- 1949-0984
- PMC
- PMC4615906
- OpenAlex
- W1964485249
- Semantic Scholar
- 10b0e7d77ac0c96917fb9e7be28852f987ee6021
- Cited by
- 296
- References
- 30
- Citations by year
- 2026: 22 · 2025: 32 · 2024: 27 · 2023: 31 · 2022: 35 · 2021: 39 · 2020: 35 · 2019: 24 · 2018: 18 · 2017: 16 · 2016: 11 · 2015: 5
- FWCI
- 7.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gut Microbes (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Institut National de la Santé et de la Recherche Médicale (USC-2018, U1071)
- Ligue Contre le Cancer
- Centre National de la Recherche Scientifique
- Institut National de la Recherche Agronomique (U1071, USC-2018)
- Centre Hospitalier Universitaire de Clermont-Ferrand
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Escherichia coli research studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biotechnology › Cancer Research and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Keywords
- colibactin, Escherichia coli, colorectal cancer, tumor microenvironment, cellular senescence, SENP1, miR-20a-5p, growth factors, gut microbiota, carcinogenesis, xenograft mouse model
- MeSH terms
- Animals, Colonic Neoplasms, Cysteine Endopeptidases, Escherichia coli, Models, Biological, Mutagens, Endopeptidases, Peptides, Tumor Suppressor Protein p53, MicroRNAs, Mice, Sumoylation, Tumor Microenvironment, Polyketides
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