Background: Desmoglein2 (DSG2) is a transmembrane protein that helps regulate intercellular connections and contributes to desmosome assembly. Desmosome are associated with cell adhesion junctions, which play an important role in cancer progression specially cancer cell migration and invasion. However, DSG2 expression in colon cancer (CC) and its association with CC patients' overall survival (OS) are still unclear.
Methods: We collected 587 CC samples, 41 colitis tissues and 114 pericarcinomatous tissues, as well as corresponding clinicopathological data about the patients who contributed them. All samples were tested immunohistochemically in tissue microarrays. Kaplan-Meier method was used for calculating patient survival. Univariate and multivariate analyses was used for investigating DGS2 link with CC patient's clinicopathological factors. Bioinformatics analysis was also used in study.
Results: The results showed that DSG2 expression was lower in CC tissues than in pericarcinomatous tissues (P < 0.001). DSG2 expression was associated with differentiation (P = 0.033), lymph node metastasis (P = 0.045), distant metastasis (P = 0.006) and AJCC stage (P < 0.001). Univariate analysis indicated that poor OS in patients with CC was associated with low DSG2 expression (P < 0.001), tumor size (P < 0.001), lymph node metastasis (P < 0.001), distant metastasis (P < 0.001), AJCC stage (P < 0.001) and venous invasion (P < 0.001). In multivariate analysis, low DSG2 expression (P < 0.001), distant metastasis (P < 0.001), AJCC stage (P = 0.002), venous invasion (P < 0.001) were independent prognostic factors for CC patients. Bioinformatics analysis indicated that low DSG2 expression affects protein activation, regulates the P53-related pathway in CC, and activates the EGFR pathway.
Conclusions: The results suggest that low DSG2 expression is associated with poor survival for CC patients. DSG2 could be a prognostic biomarker for CC.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7789404 | PMC |
http://dx.doi.org/10.1186/s12876-020-01588-2 | DOI Listing |
Arrhythmogenic cardiomyopathy (ACM) is a genetic form of heart failure that affects 1 in 5000 people globally and is caused by mutations in cardiac desmosomal proteins including , and Individuals with ACM suffer from ventricular arrhythmias, sudden cardiac death, and heart failure. There are few effective treatments and heart transplantation remains the best option for many affected individuals. Here we performed single nucleus RNA sequencing (snRNAseq) and spatial transcriptomics on myocardial samples from patients with ACM and control donors.
View Article and Find Full Text PDFNat Commun
December 2024
Department of Pulmonary and Critical Care Medicine, Ruijin Hospital, Institutes of Respiratory Diseases, School of Medicine, Shanghai Jiao Tong University and Shanghai Key Laboratory of Emergency Prevention, Diagnosis and Treatment of Respiratory Infectious Diseases, Shanghai, China.
Human adenovirus (HAdV) is a widely spread respiratory pathogen that can cause infections in multiple tissues and organs. Previous studies have established an association between HAdV species B (HAdV-B) infection and severe community-acquired pneumonia (SCAP). However, the connection between SCAP-associated HAdV-B infection and host factor expression profile in patients has not been systematically investigated.
View Article and Find Full Text PDFHum Genome Var
December 2024
Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, 565-0871, Japan.
DSG2, encoding desmoglein-2, is one of the causative genes of arrhythmogenic cardiomyopathy. We previously identified a homozygous DSG2 p.Arg119Ter stop-gain variant in a patient with juvenile-onset cardiomyopathy and advanced biventricular heart failure.
View Article and Find Full Text PDFCancer Cell Int
November 2024
Department of Radiation Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Mayo Clin Proc
November 2024
The Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN. Electronic address:
Objective: To determine the prevalence, penetrance, and disease expression of cardiomyopathy-related genetic variants in an unselected, richly phenotyped Mayo Clinic population in the setting of preemptive sequencing, with return of incidental findings following the American College of Medical Genetics and Genomics recommendations.
Patients And Methods: We analyzed a quaternary medical center-based biobank cohort (n=983) for reportable variants in 15 cardiomyopathy genes. Prioritization of genetic variants was performed using an internally developed pipeline to identify potentially reportable variants.
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