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| 1 | Gut microbiota imbalance and colorectal cancer显示文摘The gut microbiota acts as a real organ. The symbiotic interactions between resident micro-organisms and the digestive tract highly contribute to maintain the gut homeostasis. However, alterations to the microbiome caused by environmental changes(e.g., infection, diet and/or lifestyle) can disturb this symbiotic relationship and promote disease, such as inflammatory bowel diseases and cancer. Colorectal cancer is a complex association of tumoral cells, non-neoplastic cells and a large amount of micro-organisms, and the involvement of the microbiota in colorectal carcinogenesis is becoming increasingly clear. Indeed, many changes in the bacterial composition of the gut microbiota have been reported in colorectal cancer, suggesting a major role of dysbiosis in colorectal carcinogenesis. Some bacterial species have been identified and suspected to play a role in colorectal carcinogenesis, such as Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis, Enterococcus faecalis, Clostridium septicum, Fusobacterium spp. and Escherichia coli. The potential pro-carcinogenic effects of these bacteria are now better understood. In this review, we discuss the possible links between the bacterial microbiota and colorectal carcinogenesis, focusing on dysbiosis and the potential pro-carcinogenic properties of bacteria, such as genotoxicity and other virulence factors, inflammation, host defenses modulation, bacterial derived metabolism, oxidative stress and anti-oxidative defenses modulation. We lastly describe how bacterial microbiota modifications could represent novel prognosis markers and/or targets for innovative therapeutic strategies. | Johan Gagnière Jennifer Raisch Julie Veziant Nicolas Barnich Richard Bonnet Emmanuel Buc Marie-Agnès Bringer Denis Pezet Mathilde Bonnet | 2016 | World Journal of Gastroenterology2016，22，2： | 76 |
| 2 | Colon cancer-associated B2 Escherichia coli colonize gut mucosa and promote cell proliferation显示文摘AIM:To provide further insight into the characterization of mucosa-associated Escherichia coli(E.coli)isolated from the colonic mucosa of cancer patients.METHODS:Phylogroups and the presence of cyclomodulin-encoding genes of mucosa-associated E.coli from colon cancer and diverticulosis specimens weredetermined by PCR.Adhesion and invasion experiments were performed with I-407 intestinal epithelial cells using gentamicin protection assay.Carcinoembryonic antigen-related cell adhesion molecule 6(CEACAM6)expression in T84 intestinal epithelial cells was measured by enzyme-linked immunosorbent assay and by Western Blot.Gut colonization,inflammation and procarcinogenic potential were assessed in a chronic infection model using CEABAC10 transgenic mice.Cell proliferation was analyzed by real-time mRNA quantification of PCNA and immunohistochemistry staining of Ki67.RESULTS:Analysis of mucosa-associated E.coli from colon cancer and diverticulosis specimens showed that whatever the origin of the E.coli strains,86%of cyclomodulin-positive E.coli belonged to B2 phylogroup and most harbored polyketide synthase(pks)island,which encodes colibactin,and/or cytotoxic necrotizing factor(cnf)genes.In vitro assays using I-407 intestinal epithelial cells revealed that mucosa-associated B2 E.coli strains were poorly adherent and invasive.However,mucosa-associated B2 E.coli similarly to Crohn’s disease-associated E.coli are able to induce CEACAM6expression in T84 intestinal epithelial cells.In addition,in vivo experiments using a chronic infection model of CEACAM6 expressing mice showed that B2 E.coli strain11G5 isolated from colon cancer is able to highly persist in the gut,and to induce colon inflammation,epithelial damages and cell proliferation.CONCLUSION:In conclusion,these data bring new insights into the ability of E.coli isolated from patients with colon cancer to establish persistent colonization,exacerbate inflammation and trigger carcinogenesis. | Jennifer Raisch Emmanuel Buc Mathilde Bonnet Pierre Sauvanet Emilie Vazeille Amélie de Vallée Pierre Déchelotte Claude Darcha Denis Pezet Richard Bonnet Marie-Agnès Bringer Arlette Darfeuille-Michaud | 2014 | World Journal of Gastroenterology2014，20，21： | 12 |
| 3 | Silibinin induces hepatic stellate cell cycle arrest via enhancing p53/p27 and inhibiting Akt downstream signaling protein expression显示文摘BACKGROUND: Proliferation of hepatic stellate cells(HSCs) plays a pivotal role in the progression of liver fibrosis consequent to chronic liver injury. Silibinin, a flavonoid compound,has been shown to possess anti-fibrogenic effects in animal models of liver fibrosis. This was attributed to an inhibition of cell proliferation of activated HSCs. The present study was to gain insight into the molecular pathways involved in silibinin anti-fibrogenic effect. METHODS: The study was conducted on LX-2 human stellate cells treated with three concentrations of silibinin(10, 50 and 100 μmol/L) for 24 and 96 hours. At the end of the treatment cell viability and proliferation were evaluated. Protein expression of p27, p21, p53, Akt and phosphorylated-Akt was evaluated by Western blotting analysis and Ki-67 protein expression was by immunocytochemistry. Sirtuin activity was evaluated by chemiluminescence based assay. RESULTS: Silibinin inhibits LX-2 cell proliferation in doseand time-dependent manner; we showed that silibinin upregulated the protein expressions of p27 and p53. Such regulation was correlated to an inhibition of both downstream Akt and phosphorylated-Akt protein signaling and Ki-67 protein expression. Sirtuin activity also was correlated to silibinininhibited proliferation of LX-2 cells. CONCLUSION: The anti-proliferative effect of silibinin on LX-2 human stellate cells is via the inhibition of the expressions of various cell cycle targets including p27, Akt and sirtuin signaling. | Devaraj Ezhilarasan Jonathan Evraerts Brice Sid Pedro Buc Calderon Sivanesan Karthikeyan Etienne Sokal Mustapha Najimi | 2017 | Hepatobiliary & Pancreatic Diseases International2017，16，1： | 7 |
| 4 | Role of AMPK activation in oxidative cell damage: Implications for alcohol-induced liver disease显示文摘 | Brice Sid Julien Verrax Pedro Buc Calderon | 2013 | Biochemical Pharmacology2013，，2： | 3 |
| 5 | Peng's binding pancreaticojejunostomy after pancreaticoduodenectomy:a French prospective study显示文摘 | Buc E Flamein R Golfier C | 2010 | J Gastrointest Surg2010，14，： | 1 |
| 6 | Characterization of Ni O thin films deposited by reactive sputtering显示文摘 | I Hatov D Buc S Hascik | 1998 | Vacuum1998，50，12： | 1 |
| 7 | KRAS mutations as an independent prognostic factor in pa- tients with advanced colorectal cancer treated with cetuximab 显示文摘 | Lievre A Bachet J B Boige V Cayre A Le Corre D Buc E | 2008 | J Clin Oncol2008，26，： | 1 |
| 8 | Peng' s binding pancreaticcojejunostomy 'after pancreaticcododenectomy: a French prospective study显示文摘 | Buc E Flamein R Golffier C | 2010 | J Gastrointest Surgy2010，14，4： | 1 |
| 9 | Targeting cancer cells by an oxidant-based therapy显示文摘 | Verrax J Taper H Buc CP | 2008 | Curr Mol Pharmacol2008，1，： | 1 |
| 10 | Thermal Stablity of NbN Films Deposited on GaAs Substrates显示文摘 | Hotovy I Huran J Buc D el al | 1998 | Vacuum1998，50，12： | 1 |
| 11 | Peng’s binding pancreati-cojejunostomy after pancreaticoduodenectomy : a French prospec-tive study 显示文摘 | Buc E Flamein R Golffier C | 2010 | J Gastrointest Surg2010，14，4： | 1 |
| 12 | Duodenopancreatectomía cefálica显示文摘 | E. Buc A. Sauvanet | 2012 | EMC - Técnicas quirúrgicas - Aparato digestivo2012，，1： | 1 |
| 13 | An improved synthesis of P-alanine 显示文摘 | Buc SR Ford JH Wise E | 1945 | Journal of the American Chemical Society1945，67，1： | 1 |
| 14 | Occurrence rotes of HLA-DRBI and HLA-DPBI alleles in patients suffering from vitiligo 显示文摘 | Buc M Fazekasova H Cechove E | 1998 | Eur J Dermatol1998，8，1： | 1 |
| 15 | Small punch test evaluation of intergranular embrittlement of an aBoy steele显示文摘 | Baik J M Kameda J Buc O | 1983 | Script Mitalurgica1983，1，7： | 1 |
| 16 | Cerebral infarct and the immune response显示文摘 | Bartko D Lesicky O Buc M | 1997 | Bratisl Lek Listy1997，98，6： | 1 |
| 17 | Phosphofiuctokinases from Escherichia coli显示文摘 | Kotlarz D Buc H | 1982 | Methods Encymol1982，90，： | 1 |
| 18 | Peng’s Binding Pancreaticojejunostomy After Pancreaticoduodenectomy: A French Prospective Study显示文摘 | Emmanuel Buc Renaud Flamein Claudio Golffier Anne Dubois Ganesh Nagarajan Emmanuel Futier Denis Pezet | 2010 | Journal of Gastrointestinal Surgery2010，，4： | 1 |
| 19 | Changes in visual evoked potentials curve parameters in children w ith amblyopia显示文摘 | Karlica D Galetovic'D Buc'an K Znaor L Skelin S | 2009 | Acta Med Croatica2009，63，4： | 1 |
| 20 | Tobacco smoking:a factor of early onset of colorectal cancer显示文摘 | Buc E Kwiatkowski F AlvesA | 2006 | Dis Colon Rectum2006，49，12： | 1 |
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