scholarly journals Fusobacterium�nucleatum promotes the progression of colorectal cancer by interacting with E‑cadherin

2018 ◽  
Author(s):  
Chun‑Ting Ma ◽  
He‑Sheng Luo ◽  
Feng Gao ◽  
Qin‑Cai Tang ◽  
Wei Chen
Keyword(s):  
Colorectal Cancer ◽  
Fusobacterium Nucleatum ◽  
E Cadherin

scholarly journals FadA promotes DNA damage and progression of Fusobacterium nucleatum-induced colorectal cancer through up-regulation of chk2

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Pin Guo ◽  
Zibin Tian ◽  
Xinjuan Kong ◽  
Lin Yang ◽  
Xinzhi Shan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Fusobacterium Nucleatum ◽  
Immunofluorescence Assay ◽  
S Phase ◽  
Polyposis Coli ◽  
Tumor Number ◽  
E Cadherin

Abstract Background Globally, colorectal cancer (CRC) affects more than 1 million people each year. In addition to non-modifiable and other environmental risk factors, Fusobacterium nucleatum infection has been linked to CRC recently. In this study, we explored mechanisms underlying the role of Fusobacterium nucleatum infection in the progression of CRC in a mouse model. Methods C57BL/6 J-Adenomatous polyposis coli (APC) Min/J mice [APC (Min/+)] were treated with Fusobacterium nucleatum (109 cfu/mL, 0.2 mL/time/day, i.g., 12 weeks), saline, or FadA knockout (FadA−/−) Fusobacterium nucleatum. The number, size, and weight of CRC tumors were determined in isolated tumor masses. The human CRC cell lines HCT29 and HT116 were treated with lentiviral vectors overexpressing chk2 or silencing β-catenin. DNA damage was determined by Comet assay and γH2AX immunofluorescence assay and flow cytometry. The mRNA expression of chk2 was determined by RT-qPCR. Protein expression of FadA, E-cadherin, β-catenin, and chk2 were determined by Western blot analysis. Results Fusobacterium nucleatum treatment promoted DNA damage in CRC in APC (Min/+) mice. Fusobacterium nucleatum also increased the number of CRC cells that were in the S phase of the cell cycle. FadA−/− reduced tumor number, size, and burden in vivo. FadA−/− also reduced DNA damage, cell proliferation, expression of E-cadherin and chk2, and cells in the S phase. Chk2 overexpression elevated DNA damage and tumor growth in APC (Min/+) mice. Conclusions In conclusion, this study provided evidence that Fusobacterium nucleatum induced DNA damage and cell growth in CRC through FadA-dependent activation of the E-cadherin/β-catenin pathway, leading to up-regulation of chk2.

Loss of E-cadherin expression in colorectal cancer

Endoscopy ◽  
2006 ◽  
Vol 37 (12) ◽  
Author(s):  
E Fox ◽  
DT Leahy ◽  
R Geraghty ◽  
D Keegan ◽  
A White ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
E Cadherin

Fusobacterium nucleatum Promotes Colorectal Cancer Metastasis by Modulating KRT7-AS/KRT7

2019 ◽  
Author(s):  
Shujie Chen ◽  
Tingting Su ◽  
Ying Zhang ◽  
Allen Lee ◽  
Jiamin He ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Metastasis ◽  
Fusobacterium Nucleatum ◽  
Colorectal Cancer Metastasis

scholarly journals Association between colorectal cancer and Fusobacterium nucleatum and Bacteroides fragilis bacteria in Iranian patients: a preliminary study

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Aref Shariati ◽  
Shabnam Razavi ◽  
Ehsanollah Ghaznavi-Rad ◽  
Behnaz Jahanbin ◽  
Abolfazl Akbari ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Relative Abundance ◽  
Normal Tissue ◽  
Bacteroides Fragilis ◽  
Fusobacterium Nucleatum ◽  
Normal Mucosa ◽  
Clinicopathologic Characteristics ◽  
Tissue Samples ◽  
Adjacent Normal Mucosa ◽  
Iranian Patients

Abstract Background and aim Recent studies have proposed that commensal bacteria might be involved in the development and progression of gastrointestinal disorders such as colorectal cancer (CRC). Therefore, in this study, the relative abundance of Fusobacterium nucleatum, Bacteroides fragilis, Streptococcus bovis/gallolyticus, and Enteropathogenic Escherichia coli (EPEC) in CRC tissues, and their association with clinicopathologic characteristics of CRC was investigated in Iranian patients. Moreover, the role of these bacteria in the CRC-associated mutations including PIK3CA, KRAS, and BRAF was studied. Method To these ends, the noted bacteria were quantified in paired tumors and normal tissue specimens of 30 CRC patients, by TaqMan quantitative Real-Time Polymerase Chain Reaction (qPCR). Next, possible correlations between clinicopathologic factors and mutations in PIK3CA, KRAS, and BRAF genes were analyzed. Results In studied samples, B. fragilis was the most abundant bacteria that was detected in 66 and 60% of paired tumor and normal samples, respectively. Furthermore, 15% of the B. fragilis-positive patients were infected with Enterotoxigenic B. fragilis (ETBF) in both adenocarcinoma and matched adjacent normal samples. F. nucleatum was also identified in 23% of tumors and 13% of adjacent normal tissue samples. Moreover, the relative abundance of these bacteria determined by 2-ΔCT was significantly higher in CRC samples than in adjacent normal mucosa (p < 0.05). On the other hand, our findings indicated that S. gallolyticus and EPEC, compared to adjacent normal mucosa, were not prevalent in CRC tissues. Finally, our results revealed a correlation between F. nucleatum-positive patients and the KRAS mutation (p = 0.02), while analyses did not show any association between bacteria and mutation in PIK3CA and BRAF genes. Conclusion The present study is the first report on the analysis of different bacteria in CRC tissue samples of Iranian patients. Our findings revealed that F. nucleatum and B. fragilis might be linked to CRC. However, any link between gut microbiome dysbiosis and CRC remains unknown.

scholarly journals Association of Fusobacterium nucleatum infection and colorectal cancer: A Mexican study

2021 ◽  
Author(s):  
H. Cuellar-Gómez ◽  
M.E. Ocharán-Hernández ◽  
C.C. Calzada-Mendoza ◽  
D.A. Comoto-Santacruz
Keyword(s):  
Colorectal Cancer ◽  
Fusobacterium Nucleatum

Soluble serum E-cadherin as a marker of tumour progression in colorectal cancer patients

2004 ◽  
Vol 21 (1) ◽  
pp. 75-78 ◽  
Author(s):  
C. Wilmanns ◽  
J. Grossmann ◽  
S. Steinhauer ◽  
G. Manthey ◽  
B. Weinhold ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Patients ◽  
Tumour Progression ◽  
Colorectal Cancer Patients ◽  
E Cadherin

scholarly journals Epithelial-Mesenchymal Transition Phenotype, Metformin, and Survival for Colorectal Cancer Patients with Diabetes Mellitus II

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yaodu Wang ◽  
Zhiyang Wu ◽  
Likuan Hu
Keyword(s):  
Diabetes Mellitus ◽  
Colorectal Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Disease Free Survival ◽  
Multivariate Regression Analysis ◽  
Stage I ◽  
Clinicopathological Parameters ◽  
Mesenchymal Transition ◽  
Patients With Diabetes ◽  
E Cadherin

Objectives. We aimed to explore the association between metformin treatment and epithelial-mesenchymal transition (EMT) phenotype and further appraise the prognostic values of metformin and EMT markers E-cadherin and vimentin for colorectal cancer (CRC) in clinical practice. Methods. We collected specimens and evaluated clinicopathological parameters of 102 stage I to III CRC patients with prediagnosed type 2 diabetes mellitus (DM II). Expression of E-cadherin and vimentin in tumors was detected by immunohistochemistry (IHC), and statistical analysis was performed using SPSS 19.0. Results. In correlation tests, we found a lower tumor cell EMT degree (more E-cadherin (P=0.014) and less vimentin (P=0.011) expression in patients who used metformin, and the expression of E-cadherin and vimentin was associated with serum CA19-9 (P=0.048, P=0.009), tumor invasive depth (T) (P<0.001, P=0.045), and lymph invasion (N) (P=0.013, P=0.001). In Cox multivariate regression analysis, E-cadherin was identified as a prognostic factor for disease-free survival (DFS) (P=0.038) and metformin use (P=0.015P=0.044) and lymph invasion (P=0.016P=0.023) were considered as the prognostic factors for both DFS and overall survival (OS). Conclusion. Our study suggested that metformin may impede the EMT process and improve survival for stage I–III CRC patients with DM II.

E-cadherin (CDH1) gene promoter polymorphism and the risk of colorectal cancer

2011 ◽  
Vol 27 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Yadong Wang ◽  
Haiyan Yang ◽  
Li Li ◽  
Haiyu Wang ◽  
Congke Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gene Promoter ◽  
Promoter Polymorphism ◽  
Cdh1 Gene ◽  
Gene Promoter Polymorphism ◽  
E Cadherin

scholarly journals The role of Fusobacterium nucleatum in colorectal cancer: from carcinogenesis to clinical management

2019 ◽  
Vol 5 (3) ◽  
pp. 178-187 ◽  
Author(s):  
Chun-Hui Sun ◽  
Bin-Bin Li ◽  
Bo Wang ◽  
Jing Zhao ◽  
Xiao-Ying Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Clinical Management ◽  
Fusobacterium Nucleatum
Sign in / Sign up

Export Citation Format

Share Document