Claudin expression in Barrett's esophagus and adenocarcinoma

Györffy, Hajnalka; Holczbauer, Ágnes; Nagy, Péter; Szabó, Zsuzsa; Kempler, Péter; Páska, Csilla; Papp, J.; Schaff, Zsuzsa; Kiss, András

doi:10.1007/s00428-005-0045-9

Cited by 55 publications

(58 citation statements)

References 39 publications

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“…[17][18][19] In line with this hypothesis complex alterations of TJ expression in BE and BC compared to esophageal squamous epithelium have been observed: claudin-1 and claudin-5 are downregulated in BE 19,20 whereas for claudin-2, -3, -4 and -7 an upregulation has been noted, in particular in highgrade IN and BC. 17,19,21 These data suggest that downregulated TJ proteins might facilitate inhibitory functions, whereas upregulated TJs may promote the progression of BE. However, despite these findings a detailed understanding of how TJ contribute to malignant transformation and disease progression in BE and BC, is still lacking.…”

Section: Introductionmentioning

confidence: 86%

Expression and function of the coxsackie and adenovirus receptor in Barrett's esophagus and associated neoplasia

et al. 2009

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Cell surface presence of the coxsackie and adenovirus receptor (CAR) is considered a crucial prerequisite for the uptake of attenuated adenovirus. In cancers, however, a frequent loss of CAR has been noted potentially hampering the success of adenovirus-based therapy. In esophageal Barrett's carcinomas and its precursor lesions CAR presence has not been systematically determined yet. Immunohistochemical assessment in tissue specimens of 111 patients revealed CAR-positivity in all cases of Barrett's esophagus, including various degrees of intraepithelial neoplasia. In contrast, no considerable CAR presence was seen in squamous esophageal epithelium. Among Barrett's carcinomas, 93% displayed CAR presence, whereas CAR-negativity was observed preferentially in advanced cancers. Aiming to evaluate whether this loss of CAR impacts tumor-biologic properties of esophageal adenocarcinomas we studied cell lines OE19 and OE33 and observed an increased proliferation, migration and invasion upon siRNA-mediated functional CAR knock down. In conclusion, our results indicate that CAR may provide a valuable target for adenovirus-based therapy of Barrett's carcinomas and its precursor lesions. These data do also suggest that CAR does not contribute substantially to carcinogenesis in Barrett's esophagus, however, it may be speculated that loss of CAR promotes tumor progression in advanced stages of Barrett's carcinomas.

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Section: Introductionmentioning

confidence: 86%

Expression and function of the coxsackie and adenovirus receptor in Barrett's esophagus and associated neoplasia

et al. 2009

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“…Immunohistochemical analysis indicated that CLDN2 expression was increased in Barrett's esophageal cancer and that CLDN3 and CLDN4 were up-regulated in Barrett's esophagus and adenocarcinoma [40]. In contrast, another report showed upregulation of CLDN2 and CLDN3 and downregulation of CLDN1 in Barrett's esophagus [41].…”

Section: Involvement Of Tj Proteins In Diseases Gastroesophageal Reflmentioning

confidence: 95%

“…Few studies have analyzed TJ protein expression in esophageal squamous cell carcinoma; an increase in CLDN1 immunohistochemical staining, and no change in CLDN4 and CLDN7 staining, have been reported [40]. Immunohistochemical analysis indicated that CLDN2 expression was increased in Barrett's esophageal cancer and that CLDN3 and CLDN4 were up-regulated in Barrett's esophagus and adenocarcinoma [40].…”

Section: Involvement Of Tj Proteins In Diseases Gastroesophageal Reflmentioning

confidence: 99%

Gastrointestinal mucosal barrier function and diseases

2016

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The gastrointestinal mucosal barrier plays an essential role in the separation of the inside of the body from the outside environment. Tight junctions (TJs) are the most important component for construction of a constitutive barrier of epithelial cells, and they regulate the permeability of the barrier by tightly sealing the cell-cell junctions. TJ proteins are represented by claudins, occludin, junctional adhesion molecules, and scaffold protein zonula occludens. Among these TJ proteins, claudins are the major components of TJs and are responsible for the barrier and the polarity of the epithelial cells. Gastrointestinal diseases including reflux esophagitis, inflammatory bowel disease, functional gastrointestinal disorders, and cancers may be regulated by these molecules, and disruption of their functions leads to chronic inflammatory conditions and chronic or progressive disease. Therefore, regulation of the barrier function of epithelial cells by regulating the expression and localization of TJ proteins is a potential new target for the treatment of these diseases. Treatment strategies for these diseases might thus be largely altered if symptom generation and/or immune dysfunction could be regulated through improvement of mucosal barrier function. Since TJ proteins may also modify tumor infiltration and metastasis, other important goals include finding a good TJ biomarker of cancer progression and patient prognosis, and developing TJ protein-targeted therapies that can modify patient prognosis. This review summarizes current understanding of gastrointestinal barrier function, TJ protein expression, and the mechanisms underlying epithelial barrier dysregulation in gastrointestinal diseases.

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“…Several reports suggested that the claudins were correlated with esophageal cancer carcinogenesis. Significant increase in claudin-1 expression was detected in esophageal squamous cell carcinoma as compared with that in esophageal squamous epithelium (6), and reduced expression of claudin-1 was significantly associated with histological differentiation of the tumor (28). However, the relationship between the claudins and recurrence status of esophageal cancer has not yet 47-82) years.…”

mentioning

confidence: 99%

“…The claudins have been suggested to be associated with carcinogenesis and tumor progression. Alteration of claudins has been detected in carcinomas of the esophagus (6,13,15,23,28), colorectum (14,19), and other cancers (16,21,24), suggesting that the claudins are involved in the process of carcinogenesis (20).…”

mentioning

confidence: 99%

Decreased expression of claudin-1 is correlated with recurrence status in esophageal squamous cell carcinoma

et al. 2008

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Claudins are transmembrane proteins and major constitutes of tight junctions, and participate in the paracellular barrior and cellular connecting functions. They have been shown to be differentially regulated in malignant tumors and play a role in carcinogenesis and tumor progression. Recent studies have shown changes in expression of claudins during tumorigenesis. However, a causal relationship between claudin expression and cancer recurrent status has not been established. In this study, we examined 54 esophageal cancer cases to assess immunohistochemical expression patterns of claudin-1. Eleven (20.4%) of 54 cases had negative immunostaining for claudin-1. Decreased expression of claudin-1 was statistically correlated with recurrence status (P = 0.018). The cases with lymphatic vessel permeation showed reduced expression patterns of claudin-1 (P = 0.033). Decreased expression of claudin-1 was also correlated with short diseasefree survival (P = 0.0003) and overall survival (P = 0.0045). The results indicated that claudin-1 expression was correlated with the recurrence status and poor prognosis in esophageal cancer and claudin-1 expression may be a good indicator of recurrence in esophageal cancer.

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Claudin expression in Barrett's esophagus and adenocarcinoma

Cited by 55 publications

References 39 publications

Expression and function of the coxsackie and adenovirus receptor in Barrett's esophagus and associated neoplasia

Expression and function of the coxsackie and adenovirus receptor in Barrett's esophagus and associated neoplasia

Gastrointestinal mucosal barrier function and diseases

Decreased expression of claudin-1 is correlated with recurrence status in esophageal squamous cell carcinoma

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