Expression patterns of dysadherin and E-cadherin in lymph node metastases of colorectal carcinoma

Batistatou, Anna; Charalabopoulos, Alexander; Scopa, Chrisoula D.; Nakanishi, Yukihiro; Kappas, Angelos M.; Hirohashi, Setsuo; Agnantis, Niki J.; Charalabopoulos, Konstantinos

doi:10.1007/s00428-006-0183-8

Cited by 33 publications

(28 citation statements)

References 37 publications

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“…LEPR was associated with pituitary adenoma, 12,20,46 FXYD5 was associated with a broad spectrum of cancers, and KCNMA1 was also associated with giloma. 3,19,27,41 The number of overlapping genes between each pair of the 3 data sets was higher: 26 between the UCLA and USC studies, 34 between the Scheck and USC studies, and 35 between the UCLA and Scheck studies. Interestingly, we found that the MN1 gene was also differentially expressed in the UCLA data set.…”

Section: Gene Expression Analysismentioning

confidence: 96%

Genomic and transcriptome analysis revealing an oncogenic functional module in meningiomas

Chang

Shi

Russin

et al. 2013

FOC

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Object Meningiomas are among the most common primary adult brain tumors. Although typically benign, roughly 2%–5% display malignant pathological features. The key molecular pathways involved in malignant transformation remain to be determined. Methods Illumina expression microarrays were used to assess gene expression levels, and Illumina single-nucleotide polymorphism arrays were used to identify copy number variants in benign, atypical, and malignant meningiomas (19 tumors, including 4 malignant ones). The authors also reanalyzed 2 expression data sets generated on Affymetrix microarrays (n = 68, including 6 malignant ones; n = 56, including 3 malignant ones). A weighted gene coexpression network approach was used to identify coexpression modules associated with malignancy. Results At the genomic level, malignant meningiomas had more chromosomal losses than atypical and benign meningiomas, with average length of 528, 203, and 34 megabases, respectively. Monosomic loss of chromosome 22 was confirmed to be one of the primary chromosomal level abnormalities in all subtypes of meningiomas. At the transcriptome level, the authors identified 23 coexpression modules from the weighted gene coexpression network. Gene functional enrichment analysis highlighted a module with 356 genes that was highly related to tumorigenesis. Four intramodular hubs within the module (GAB2, KLF2, ID1, and CTF1) were oncogenic in other cancers such as leukemia. A putative meningioma tumor suppressor MN1 was also identified in this module with differential expression between malignant and benign meningiomas. Conclusions The authors' genomic and transcriptome analysis of meningiomas provides novel insights into the molecular pathways involved in malignant transformation of meningiomas, with implications for molecular heterogeneity of the disease.

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Section: Gene Expression Analysismentioning

confidence: 96%

Genomic and transcriptome analysis revealing an oncogenic functional module in meningiomas

Chang

Shi

Russin

et al. 2013

FOC

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“…It is estimated that dysadherin expression would be a good biological predictor for cell invasion and metastasis in human cancers (Hirohashi and Kanai 2003;Shimamura et al 2004). It was reported that dysadherin expression has prognostic importance in advanced colorectal cancers (Batistatou et al 2006). Dysadherin is also known as Fxyd domain containing ion transport regulator 5 (FXYD5).…”

Section: Introductionmentioning

confidence: 99%

Alterations in dysadherin expression and F-actin reorganization: a possible mechanism of hypericin-mediated photodynamic therapy in colon adenocarcinoma cells

2014

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Dysadherin is a recently found anti-adhesion molecule, therefore detection and down regulation of its expression is promising in cancer treatment. The up-regulation of dysadherin contributes to colon cancer recurrence and metastasis. Dysadherin also has connections with cytoskeletal proteins and it can cause alterations in the organisation of filamentous actin (Factin) in metastatic cancers. In this study, hypericin (HYP)-mediated photodynamic therapy (PDT) was performed in two different grade colon adenocarcinoma cell lines HT-29 (Grade I) and Caco-2 (Grade II). Cells were treated with 0.04, 0.08 or 0.15 lM HYP concentrations and irradiated with (4 J/cm 2 ) fluorescent lamps. The effects of HYP was examined 16 and 24 h after the activation. We investigated for the first time the effect of HYP-mediated PDT on the expression of dysadherin and F-actin organisation. According to the results, HYP mediated PDT caused a decrease in gene expression and immunofluorescence staining of dysadherin and an increase in actin stress fibers and actin aggregates in HT-29 and Caco-2 cell lines. Besides, cytotoxicity, number of floating cells and apoptotic index changed depending on the cell type, HYP concentration and incubation time. We have demonstrated for the first time that dysadherin and F-actin could be target molecules for HYP-

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“…[6][7][8] While the role of dysadherin in gastric cancer has been studied in detail, in oesophageal cancer its role remains mainly unexplored. 7,9,10 In a clinical study from Shimada et at 11 expression of dysadherin was studied in 117 patients with oesophageal squamous cell carcinoma of all stages.…”

mentioning

confidence: 99%

“…In accordance to what has been shown in relevant studies exploring the role of dysadherin in extraoesophageal human cancers, multivariate analysis revealed that in squamous cell carcinomas of the oesophagus, although expression of E-cadherin is not an independent prognostic factor, expression of dysadherin is (p<0.05). 6,11 At present and in contrary to E-cadherin, there is no research investigating the association of dysadherin with oesophageal adenocarcinoma. 12 This is particularly important in the West, where adenocarcinoma subtype comprises more than 80% of oesophageal cancers.…”

mentioning

confidence: 99%

Dysadherin: A Novel Oncogenic Molecular Biomarker in Oesophageal Cancer

Charalabopoulos¹,

Liakakos²

2017

Cancer Stud Mol Med Open J

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Dysadherin or FXYD5 is a transmembrane glycoprotein, identified for the first time in 2002 by a team of Japanese researchers. 1 Although, it is generally accepted that most of its action is derived from the increased maximal velocity (V max ) of the Na + -K + -ATPase that promotes, there are several actions of dysadherin that cannot be attributed to its interaction with the Na + -K + -ATPase. 2 Dysadherin is a well-described cancer-associated protein and a potential oncogenic molecular target with promising future significances. It has been distinctly shown, in both the cases of in vivo and in vitro studies, that when expressed in malignant tumours, it signifies augmented tumorigenesis with enhanced metastatic potential and haematogenous spread and is thus linked to poor prognosis. 3,4 On the contrary, studies based on human cancer cell lines have demonstrated that introduction of small interfering RNA (siRNA) against dysadherin leads to downregulation and subsequent membranous underexpression of dysadherin, instigating accordingly decreased collective and individual cell motility with subsequent inhibition of tumour aggressiveness and metastatic potential. 5 Its main interaction in carcinogenesis takes place with E-cadherin (epithelial cadherin); the most important adhesion molecules of the cadherin family. E-cadherin is involved in cancer development in more than 90% of human cancers, as most are carcinomas of epithelial origin. E-cadherin mediates homophilic cell-to-cell adhesion and promotes adherence between neighboring epithelial cells; its decreased cellular expression is hence associated with enhanced disconnection and dispersal of epithelial cells, promoting cell detachment from the primary lesion and consequently exhibiting increased metastatic potential.Dysadherin and its closely related E-cadherin, has been studied in various cancers and its correlation with cancer aggressiveness and poor prognosis has been collectively and undoubtedly reported. 6-8 While the role of dysadherin in gastric cancer has been studied in detail, in oesophageal cancer its role remains mainly unexplored. 7,9,10 In a clinical study from Shimada et at 11 expression of dysadherin was studied in 117 patients with oesophageal squamous cell carcinoma of all stages. The correlation between immunohistochemically evaluated dysadherin expression with patient clinicopathological data was studied. Oesophageal tumours with expression of dysadherin, displayed worse prognosis in comparison to tumours negative for dysadherin. When dysadherin positivity was combined with absence of E-cadherin expression, a statistically significant detrimental effect was exhibited in that patient group, revealing the worst prognosis of all patient groups. In the group of oesophageal tumours expressing both dysadherin and E-cadherin, prognosis was slightly better, but still poorer compared to the group of tumours that displayed no dysadherin expression. In accordance to what has been shown in relevant studies exploring the role of dysadherin in extraoesophage...

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Expression patterns of dysadherin and E-cadherin in lymph node metastases of colorectal carcinoma

Cited by 33 publications

References 37 publications

Genomic and transcriptome analysis revealing an oncogenic functional module in meningiomas

Genomic and transcriptome analysis revealing an oncogenic functional module in meningiomas

Alterations in dysadherin expression and F-actin reorganization: a possible mechanism of hypericin-mediated photodynamic therapy in colon adenocarcinoma cells

Dysadherin: A Novel Oncogenic Molecular Biomarker in Oesophageal Cancer

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