Claudins and gastric carcinogenesis

Iravani, Omid; Tay, Benjamin Wei-Rong; Chua, Pei‐Jou; Yip, George; Bay, Boon‐Huat

doi:10.1177/1535370213477981

Cited by 22 publications

(9 citation statements)

References 55 publications

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“…In conclusion, these studies revealed that alterations in the expression of claudin proteins are associated with tumorigenic growth and progression [ 45 , 46 ]. However, at present, few studies have examined the functional association between nasopharyngeal carcinogenesis and alterations in claudin protein expression [ 47 – 50 ]. In the future, we will address the specific mechanism that is responsible for our observations on how alterations in claudin protein expression affect the malignant and oncogenic phenotype of nasopharyngeal carcinoma.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Differences in the expression profiles of claudin proteins in human nasopharyngeal carcinoma compared with non-neoplastic mucosa

Zhang

Wang

et al. 2018

Diagn Pathol

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BackgroundSeveral studies have suggested that claudin proteins, which are the main components of tight junction structures, are related to the regulation of cell polarity and cell differentiation.MethodTo explore the expression profiles of the tight junction proteins claudin-2, − 5, − 8 and − 9 in nasopharyngeal carcinoma, IHC (immunohistochemical analysis), Western blot and real-time PCR were used to detect the expression profiles of these claudin proteins in nasopharyngeal carcinoma tissues and in non-neoplastic mucosal tissues.ResultsAccording to our study, the expression levels of claudin-2 and claudin-5 were reduced, while the expression of claudin-8 was increased in nasopharyngeal carcinoma tissues in comparison with non-neoplastic mucosal tissues. Correlations between claudin-2 and -5 expression and metastatic progression in nasopharyngeal carcinoma patients were also found.ConclusionIn summary, our research reveals distinct expression profiles of claudin-2, − 5 and − 8 in non-neoplastic mucosal tissues and nasopharyngeal carcinoma tissues. In addition, the expression of these claudin proteins was highly correlated with metastatic progression and prognosis in patients with nasopharyngeal carcinoma and had predictive value for the metastasis and survival of nasopharyngeal carcinoma patients.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Differences in the expression profiles of claudin proteins in human nasopharyngeal carcinoma compared with non-neoplastic mucosa

Zhang

Wang

et al. 2018

Diagn Pathol

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“…Upregulation of MT1-MMP can effectively elevate invasiveness in human cancer cells, including gastric cancer (24–26). However, to be active, the zymogens of MT1-MMP or VEGF must be cleaved from the propeptides by the protein convertase furin (7,9,27).…”

Section: Discussionmentioning

confidence: 99%

Role of c-Src activity in the regulation of gastric cancer cell migration

et al. 2014

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Gastric cancer is associated with increased migration and invasion. In the present study, we explored the role of c-Src in gastric cancer cell migration and invasion. BGC-823 gastric cancer cells were used to investigate migration following treatment of these cells with the c-Src inhibitors, PP2 and SU6656. Migration and invasion were analyzed by wound healing and Transwell assays. Western blot analysis was used to detect the expression of MT1-MMP and VEGF-C, while the activity of MMP2 and MMP9 was monitored with gelatin zymography assay. Immunoprecipitation was used to detect interactions among furin, pro-MT1-MMP and pro-VEGF-C. MT1-MMP and VEGF-C expression levels were inhibited by PP2 and SU6656 treatment, in accordance with decreased c-Src activity. Similarly, the zymography assay demonstrated that the activity of MMP2 and MMP9 was decreased following PP2 or SU6656 treatment. Blockade of c-Src also inhibited the invasive and migratory capacity of BGC-823 cells. Notably, c-Src interacted with furin in vivo, while interactions between furin and its substrates, pro-MT1-MMP and pro-VEGF-C, were decreased by c-Src inhibitors. In conclusion, the interaction among furin and pro-MT1-MMP or pro-VEGF-C or other tumor-associated precursor enzymes can be regulated by c-Src activity, thus reducing or changing the expression of these enzymes in order to reduce the development of gastric cancer, invasion and metastasis.

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“…Based on tumor biology, down-regulation of CLDN1 would result in destruction of tight junctions and loss of cell-to-cell adhesion causing tumor progression [33], however the clinical significance in gastric carcinogenesis is more complex. There is evidence that several of the claudins, CLDN1 included, show increasing levels as gastric epithelium progresses to intestinal metaplasia and early gastric carcinoma [34]. CLDN1 might influence intracellular signalling, demonstrated by Liu et al who showed that elevated expression of CLDN1 in breast cancer cells contributed to an anti-apoptotic effect through two mechanisms: inhibition of caspase-8 cleavage, and activation of the Wnt/β-catenin signal pathway [35].…”

Section: Discussionmentioning

confidence: 99%

Up-regulation of CLDN1 in gastric cancer is correlated with reduced survival

et al. 2013

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BackgroundThe genetic changes in gastric adenocarcinoma are extremely complex and reliable tumor markers have not yet been identified. There are also remarkable geographical differences in the distribution of this disease. Our aim was to identify the most differentially regulated genes in 20 gastric adenocarcinomas from a Norwegian selection, compared to matched normal mucosa, and we have related our findings to prognosis, survival and chronic Helicobacter pylori infection.MethodsBiopsies from gastric adenocarcinomas and adjacent normal gastric mucosa were obtained from 20 patients immediately following surgical resection of the tumor. Whole genome, cDNA microarray analysis was performed on the RNA isolated from the sample pairs to compare the gene expression profiles between the tumor against matched mucosa. The samples were microscopically examined to classify gastritis. The presence of H. pylori was examined using microscopy and immunohistochemistry.Results130 genes showed differential regulation above a predefined cut-off level. Interleukin-8 (IL-8) and Claudin-1 (CLDN1) were the most consistently up-regulated genes in the tumors. Very high CLDN1 expression in the tumor was identified as an independent and significant predictor gene of reduced post-operative survival. There were distinctly different expression profiles between the tumor group and the control mucosa group, and the histological subsets of mixed type, diffuse type and intestinal type cancer demonstrated further sub-clustering. Up-regulated genes were mapped to cell-adhesion, collagen-related processes and angiogenesis, whereas normal intestinal functions such as digestion and excretion were associated with down-regulated genes. We relate the current findings to our previous study on the gene response of gastric epithelial cells to H. pylori infection.ConclusionsCLDN1 was highly up-regulated in gastric cancer, and CLDN1 expression was independently associated with a poor post-operative prognosis, and may have important prognostic value. IL-8 and CLDN1 may represent central links between the gene response seen in acute H. pylori infection of gastric epithelial cells, and ultimately gastric cancer.

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Claudins and gastric carcinogenesis

Cited by 22 publications

References 55 publications

RETRACTED ARTICLE: Differences in the expression profiles of claudin proteins in human nasopharyngeal carcinoma compared with non-neoplastic mucosa

RETRACTED ARTICLE: Differences in the expression profiles of claudin proteins in human nasopharyngeal carcinoma compared with non-neoplastic mucosa

Role of c-Src activity in the regulation of gastric cancer cell migration

Up-regulation of CLDN1 in gastric cancer is correlated with reduced survival

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