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Epithelial barrier dysfunction in lymphocytic colitis occurs through downregulation of claudin-4, -5, and -8, and redistribution of claudin-5 and -8 off the tight junction, which contributes to diarrhea by a leak-flux mechanism.
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Claudin-4 expression can be absent or very focal in a subset of high-grade endometrial carcinomas
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these results suggest that Helicobacter pylori lipopolysaccharide induces TLR2 expression in the gastric adenocarcinoma cells, and that the longer the exposure to lipopolysaccharide, the greater the expression of TLR2 in the cell membrane; consequently the expression of claudin-4, -6, -7 and -9 also increases
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HIF-1alpha expression was upregulated in the vasculogenic mimicry-positive CRC cell line HCT-116 and thereby affected the expression of the EMT-related markers Claudin-4, E-cadherin (E-cd) and Vimentin(VIM).
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expression of claudin-4 is highly specific for true epithelial differentiation and may be useful to distinguish SWI/SNF complex-deficient undifferentiated carcinomas from sarcomas with epithelioid morphology. The lack of claudin-4 expression in ovarian small cell carcinomas of hypercalcemic type suggests that these tumors may be better regarded as sarcomas rather than carcinomas.
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Data indiate a regulatory network in gastric cancer whereby claudin-4 expression is reduced by specific miRNAs, which are in turn bound by specific lncRNAs acting as competing endogenous RNAs (ceRNAs), resulting in increased claudin-4 expression.
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This is the first study to show how TGF-beta regulates the expression of Claudin-4 through c-Jun signaling and how this pathway contributes to the migratory and tumorigenic phenotype of lung tumor cells.
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Claudin-4 functionally contributes to both ovarian tumor cell apoptosis resistance and migration and targeting extracellular loop interactions of claudin-4 may have therapeutic implications for reducing ovarian tumor burden.
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Fluorescence-based flow cytometry and xenon magnetic resonance imaging (MRI) indicate binding of the biosensor specifically to claudin 4 (Cldn4)-expressing cells.
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Studies indicate that Grainyhead-like transcription factor 2 (GRHL2) controls the expression of E-cadherin (CDH1) required for adherens junctions and possibly regulates the expression of claudin-4 (CLDN4) in tight junctions.
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Studies indicate claudin 1 (CLDN-1) as a target for improving epidermal drug absorption and preventing HCV infection and of claudin 4 (CLDN-4) as a target for anticancer therapeutics.
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Mislocalization claudin-3 to nucleus in colon cancer and mislocalization claudin-4 to nucleus in adenomas of the colon were detected for the first time. The potential reasons for the paradoxical expression are discussed and a review of the literature, related all the alleged mechanisms of this mislocalization is provided.
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Reg I may play a role in the maintenance of mucosal barrier function by inducing tight junction proteins such as claudins 3 and 4.
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claudin-4 may represent different mechanisms of lymphatic vessel invasion with both biomarkers is related to poor prognosis
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These results suggested that increase of Cldn4-expression may be involved in early molecular events during carcinogenesis of adenocarcinoma, whereas increase of Cldn7-expression may be associated with tumor invasion or progression.
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that claudins-4 and -7 might be valuable markers for distinguishing hepatocellular carcinoma and cholangiocarcinoma and that cholangiolocellular carcinoma might arise from hepatic ductal cells
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that claudin-4 can be helpful at least in making a reliable differential diagnosis of spiradenoma when overlapping morphologic features do not allow to further subclassification in the overwhelming variety of the adnexal tumors.
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Results showed overexpression of CLDN4 in endometrial cancer cells. Its intracellular presence coupled with the biphasic effects of E2 on its expression in the cytoskeleton suggest that it may be involved in cell signaling to and from tight junctions.
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claudin 1 and claudin 4 are differentially involved in atopic dermatitis pathogenesis
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Results suggested that claudin-4, which was regulated by methylation status, plays an important role in breast cancer growth and malignancy via the control of cell proliferation, migration and apoptosis.
