Tumor necrosis factor α stimulates invasion of Src-activated intestinal cells

Kawai, Naoki; Tsuji, S.; Tsujii, Masahiko; Ito, Toshifumi; Yasumaru, Masakazu; Kakiuchi, Yohei; Kimura, Atsuomi; Komori, Masato; Sasaki, Yutaka; Hayashi, Norio; DuBois, Raymond N.; Hori, Masatsugu

doi:10.1053/gast.2002.31023

Cited by 33 publications

(30 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…7,53) In addition, TNF-α increases peroxide production. 50) Infiltrated mast cells can up-regulate tumor angiogenesis. 54) Our findings on mast cells may suggest a need for further work to investigate the involvement of mast cells in colitis and colitis-related colon carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

A novel inflammation‐related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate

et al. 2003

View full text Add to dashboard Cite

To develop an efficient animal model for colitis-related carcinogenesis, male Crj: CD-1 (ICR) mice were given a single intraperitoneal administration (10 mg/kg body weight) of a genotoxic colonic carcinogen, azoxymethane (AOM), and a 1-week oral exposure (2% in drinking water) to a non-genotoxic carcinogen, dextran sodium sulfate (DSS), under various protocols. At week 20, colonic neoplasms (adenocarcinomas, 100% incidence with 5.60 ± ± ± ±2.42 multiplicity; and adenomas, 38% incidence with 0.20 ± ± ± ±0.40 multiplicity) with dysplastic lesions developed in mice treated with AOM followed by DSS. Protocols in which AOM was given during or after DSS administration induced a few tubular adenomas or no tumors in the colon. Immunohistochemical investigation of such dysplasias and neoplasms revealed that all lesions were positive for β β β β-catenin, cyclooxygenase-2 and inducible nitric oxide synthase, but did not show p53 immunoreactivity. The results indicate that 1-week administration of 2% DSS after initiation with a low dose of AOM exerts a powerful tumor-promoting activity in colon carcinogenesis in male ICR mice, and may provide a novel mouse model for investigating colitis-related colon carcinogenesis and for identifying xenobiotics with modifying effects. (Cancer Sci 2003; 94: 965-973) n the developed world, colorectal cancer (CRC) is one of the commonest non-smoking related cancers. This malignancy is one of the most serious complications of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), 1,2) and the risk of CRC increases with increasing extent and duration of the disease.Animal experiments are assumed to simulate or at least provide plausible pathophysiological mechanisms in various diseases including cancer and inflammatory disorders. For IBD and IBD-related CRC, several animal models have been reported. The most widely used is a mouse model with dextran sodium sulfate (DSS).3) There are a number of reports on modifying effects of xenobiotics on CRC-related colon carcinogenesis in this model 4,5) : folic acid, short chain fatty acid (butyrate), ursodeoxycholic acid, nonsteroidal anti-inflammatory drugs (NSAIDs)/cyclooxygenase (COX)-2 inhibitors, and 5-aminosalicylic acid (5-ASA) were found to inhibit the occurrence of UC-related CRC. However, this colitis model using DSS with or without carcinogen needs a long period or repeated administration of DSS to induce colitis and colitis-related CRC, and the incidence and/or multiplicity of induced tumors are relatively low.6) Many studies have suggested that chronic or repeated mucosal inflammation may result in carcinogenesis through mechanisms such as induction of genetic mutations, increased cryptal cell proliferation, changes in crypt cell metabolism, changes in bile acid enterohepatic circulation, and alterations in bacteria flora. 7,8) These ideas are consistent with the hypothesis that chronic inflammation could be associated with epithelial malignant neoplasia in the large bowel. 8) We recently reported c...

show abstract

Section: Discussionmentioning

confidence: 99%

A novel inflammation‐related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate

et al. 2003

View full text Add to dashboard Cite

show abstract

“…Interestingly, expression of v-Src in a colorectal carcinomaderived cell line resulted in anchorage-independent growth and increased motility and invasiveness; however, these cells required activation of a second signaling pathway to obtain a complete mesenchymal phenotype. Incubation with tumor necrosis factor a exacerbated the motility and invasiveness of these cells and resulted in cell scattering and the down-regulation of E-cadherin (72).…”

Section: Reconciling the Paradox Of Well-differentiated Malignant Carmentioning

confidence: 99%

Reassessing Epithelial to Mesenchymal Transition as a Prerequisite for Carcinoma Invasion and Metastasis

Christiansen

Rajasekaran²

2006

Cancer Research

938

821

View full text Add to dashboard Cite

For most carcinomas, progression toward malignancy is accompanied by loss of epithelial differentiation and a shift towards a mesenchymal phenotype. This process, referred to as epithelial to mesenchymal transition (EMT), exacerbates motility and invasiveness of many cell types and is often considered a prerequisite for tumor infiltration and metastasis. However, there are numerous examples of advanced carcinomas that adopt some mesenchymal features, yet retain characteristics of well-differentiated epithelial cells. We provide a review of these reports and describe mechanisms to explain the morphologic and molecular heterogeneity and plasticity of malignant carcinoma cells, including incomplete EMT, reversion to an epithelial phenotype, and collective migration. We suggest that these mechanisms can manifest in a series of independent and reversible steps and that EMT represents just one mechanism in the global metastatic carcinoma development process. (Cancer Res 2006; 66(17): 8319-26)

show abstract

“…The pro-inflammatory cytokine TNF-a is produced by inflammatory cells and mediates phosphorylation of the b-catenin-E-cadherin complex. These phosphorylated complexes have a decreased affinity for E-cadherin molecules on other cells and phosphorylation enhances its degradation [88]. In Barrett's esophagus, Ecadherin levels decrease along the metaplasia-dysplasiacarcinoma sequence [56,57,89].…”

Section: Loss Of Cell-cell Adhesionmentioning

confidence: 99%

Molecular alterations during development of esophageal adenocarcinoma

et al. 2005

View full text Add to dashboard Cite

The incidence of esophageal adenocarcinoma has risen significantly over the last decades. During esophageal carcinogenesis many molecular alterations occur that disrupt essential cellular processes, directing the cell to a rapidly proliferating, immortal state. The chronic inflammation that is present in Barrett's esophagus creates an environment in which such molecular alterations are both induced and tolerated. Here, the novel insights in the molecular mechanisms that underlie the development of esophageal adenocarcinoma are reviewed, focusing on the role of inflammation, angiogenesis, apoptosis inhibition, loss of cell cycle control, and loss of cell-cell adhesion. These novel developments will open new perspectives for diagnosis, treatment, and prevention of esophageal adenocarcinoma.

show abstract

Tumor necrosis factor α stimulates invasion of Src-activated intestinal cells

Cited by 33 publications

References 34 publications

A novel inflammation‐related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate

A novel inflammation‐related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate

Reassessing Epithelial to Mesenchymal Transition as a Prerequisite for Carcinoma Invasion and Metastasis

Molecular alterations during development of esophageal adenocarcinoma

Contact Info

Product

Resources

About