This study was aimed to investigate the expressions of E-cadherin, p120ctn, β-catenin and NF-κB in ulcerative colitis (UC) tissues and the implications of their expressions in the pathogenesis of UC. The expressions of E-cadherin, p120ctn, β-catenin and NF-κB were detected by immunohistochemistry, and those of p120ctn and NF-κB by Western blotting in 23 cases of UC and 17 cases of normal colonic tissues. The relationship between the expression of E-cadherin or NF-κB and that of p120ctn was analyzed by Spearman rank correlation analysis. The results showed that in UC and normal colonic groups, the abnormal expression rate of E-cadherin, p120ctn, β-catenin, and NF-κB was 52.2% vs. 0 (P<0.05), 73.9% vs. 23.5% (P<0.05), 65.2% vs. 17.6% (P<0.05) and 78.4% vs. 23.5% (P<0.05), respectively. p120ctn expression was positively correlated with E-cadherin expression (r=0.404, P<0.05), but negatively with nuclear NF-κB expression (r= - 0.347, P<0.05). Western blotting showed that as compared with the normal controls, the p120ctn protein level was significantly decreased (P<0.05), whereas the NF-κB protein level was increased (P<0.05) in UC tissues. It was concluded that in the colonic tissues of UC patients, the expressions of E-cadherin, p120ctn and β-catenin are decreased, suggesting the mucosal barrier is impaired in UC. Moreover, NF-κB is increased and activated in the UC tissues, resulting in the inflammation in UC. p120ctn may influence the UC development through modulating intercellular adhesion and inflammatory response.
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http://dx.doi.org/10.1007/s11596-015-1439-9 | DOI Listing |
Sci Adv
November 2024
Lung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Severe asthma induces substantial mortality and chronic disability due to intractable airway obstruction, which may become resistant to currently available therapies including corticosteroids and β-adrenergic agonist bronchodilators. A key effector of these changes is exaggerated airway smooth muscle (ASM) cell contraction to spasmogens. No drugs in clinical use effectively prevent ASM hyperresponsiveness in asthma across all severities.
View Article and Find Full Text PDFJ Appl Oral Sci
October 2024
Xiamen Medical College, Department of Stomotology, Xiamen 361000, China.
Objective: This study aims to explore the effects of miR-223-3p and miR-155-5p on epithelial-mesenchymal transition (EMT) and migration in oral squamous cell carcinoma (OSCC).
Methodology: EMT markers (E-cadherin, N-cadherin, P120 catenin (P120ctn), and vimentin) expression was determined by qRT-PCR and western blot analysis in SCC-9 cells which overexpress miR-155-5p and/or not express miR-223-3p. Scratch assays and Transwell migration assays were conducted to evaluate cell migration ability.
J Tradit Chin Med
August 2024
Department of spleen and stomach diseases, First Affiliated Hospital of Hebei University of Traditional Chinese Medicine, Shijiazhuang 050000, China.
Gastric Cancer
July 2024
Gastroenterology, Fundació de Recerca Clínic Barcelona-Institut d'Investigacions Biomèdiques August Pi I Sunyer (FRCB-IDIBAPS), CIBEREHD, Universitat de Barcelona, Hospital Clínic, Villarroel 170, 08036, Barcelona, Spain.
Background: CDH1 and CTNNA1 remain as the main genes for hereditary gastric cancer. However, they only explain a small fraction of gastric cancer cases with suspected inherited basis. In this study, we aimed to identify new hereditary genes for early-onset gastric cancer patients (EOGC; < 50 years old).
View Article and Find Full Text PDFBiochim Biophys Acta Mol Cell Res
June 2024
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Chonnam National University, Gwangju 61186, Republic of Korea. Electronic address:
Prostate cancer (PCa) is the second leading cause of death in males. It has been reported that δ-catenin expression is upregulated during the late stage of prostate cancer. Palmitoylation promotes protein transport to the cytomembrane and regulates protein localization and function.
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