Research Paper Volume 13, Issue 13 pp 17768—17788
Methylation silencing CDH23 is a poor prognostic marker in diffuse large B-cell lymphoma
- 1 Department of Lymphoma, Beijing Shijitan Hospital, Capital Medical University, Haidian 100038, Beijing, China
Received: January 30, 2021 Accepted: May 17, 2021 Published: July 12, 2021https://doi.org/10.18632/aging.203268
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Copyright: © 2021 Cao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Cadherin-23(CDH23) mediates homotypic and heterotypic cell-cell adhesions in cancer cells. However, the epigenetic regulation, the biological functions, the mechanisms and the prognostic value of CDH23 in diffuse large B-cell lymphoma (DLBCL) are still unclear. The Gene Expression Profiling Interactive Analysis (GEPIA) and the Gene Expression Omnibus (GEO) database were employed to analyze the CDH23 expression level in DLBCL. The correlation of CDH23 expression and methylation was analyzed by LinkedOmics database. The prognostic value was analyzed via GEPIA. Correlated genes, target kinase, target miRNA, target transcription factor and biological functions were identified by LinkedOmics and GeneMANIA database. The relationship between CDH23 and the immune cell infiltration was explored by the Tumor Immune Estimation Resource (TIMER). The expression of CDH23 was reduced by DNA methylation significantly in DLBCL tissue. Reduction of CDH23 represented poor outcome of DLBCL patients. Functional enrichment analysis showed that CDH23 mainly enriched in cancer cell growth, cell metastasis, cell adhesion, cell cycle, drug catabolic process, leukocyte mediated immunity and DNA repair by some cancer related kinases, miRNAs and transcription factors. These results indicated that methylated reduction of CDH23 represented poor outcome of DLBCL. CDH23 is associated with essential biological functions and key molecules in DLBCL. CDH23 may play crucial roles in DLBCL tumorigenesis. Our results lay a foundation for further investigation of the role of CDH23 in DLBCL tumorigenesis.
CDH23: cadherin-23; DLBCL: diffuse large B-cell lymphoma; GEPIA: Gene Expression Profiling Interactive Analysis; GEO: Gene Expression Omnibus; TIMER: Tumor Immune Estimation Resource; OS: overall survival; DFS: disease-free survival; CDK1: cyclin dependent kinase 1; CDK2: cyclin dependent kinase 2; E2F1: E2F transcription factor 1; E2F4: E2F transcription factor 4; OSGIN1: oxidative stress induced growth inhibitor 1; ANKRD2: ankyrin repeat domain 2; CAPG: capping actin protein, gelsolin like; SLITRK4: SLIT and NTRK like family member 4; ACOX2: acyl-CoA oxidase 2; EXPH5: Exophilin 5; FARP1: FERM, ARH/RhoGEF and pleckstrin domain protein 1; KRT85: keratin 85; MYO3A: myosin IIIA; SERINC1: serine incorporator 1; TAS2R39: taste 2 receptor member 39; AFDN: Afadin, adherens junction formation factor; C7: complement C7; CCN4: cellular communication network factor 4; LCNL1: lipocalin like 1; CLCN7: chloride voltage-gated channel 7; GPR153: G protein-coupled receptor 153; SLC27A1: solute carrier family 27 member 1; CDK18: cyclin dependent kinase 18; DDX52: DExD-box helicase 52; TOP2A: DNA topoisomerase II alpha; PTPDC1: protein tyrosine phosphatase domain containing 1; FPKM: Fragments Per Kilobase of exon model per Million mapped fragments.