Losing the E-cadherin plays an important role in the metastasis of cancer. The regulation of the expression of E-cadherin is unclear. Circadian rhythm alteration is associated with the pathogenesis of a number of cancers. This study aims to investigate the role of one of the circadian proteins, period-2 (Per2) in repressing the expression of E-cadherin in esophageal cancer (esophageal cancer). We observed that the levels of circadian protein Per2 were significantly increased and E-cadherin was significantly decreased in the tissue of human esophageal cancer with metastasis as compared with non-metastatic esophageal cancer. Overexpression of Per2 in the esophageal cancer cells markedly repressed the expression of E-cadherin. The pHDAC1 was detected in human esophageal cancer with metastasis, which was much less in the esophageal cancer tissue without metastasis. Overexpression of Per2 increased the levels of pHDAC1 as well as the E-cadherin repressors at the E-cadherin promoter locus. Overexpression of Per2 markedly increased the migratory capacity of esophageal cancer cells, which was abolished by the inhibition of HDAC1. We conclude that Per-2 plays an important role in the esophageal cancer cell metastasis, which may be a novel therapeutic target for the treatment of esophageal cancer.
Glioblastoma multiforme (GBM) is one of the most lethal and damaging types of human cancer. The current study was conducted to identify differentially methylated genes (DMGs) between GBM and normal controls, and to improve our understanding of GBM at the epigenetic level. The DNA methylation profile of GBM was downloaded from the Gene Expression Omnibus (GEO) database using the accession number GSE50923. The MethyAnalysis package was applied to identify DMGs between GBM and controls, which were then analyzed by functional enrichment analysis. Protein-protein interaction (PPI) networks were constructed using the hypermethylated and hypomethylated genes. Finally, transcription factors (TFs) that can regulate the hypermethylated and hypomethylated genes were predicted, followed by construction of transcriptional regulatory networks. Furthermore, another relevant dataset, GSE22867, was downloaded from the GEO database for data validation. A total of 476 hypermethylated and 850 hypomethylated genes were identified, which were mainly associated with the functions of ‘G-protein-coupled receptors ligand binding’, ‘cytokine activity’, ‘cytokine-cytokine receptor interaction’, and ‘D-glutamine and D-glutamate metabolism’. The hypermethylated gene neuropeptide Y ( NPY ) and the hypomethylated gene tumor necrosis factor ( TNF ) demonstrated high degrees in the PPI network. Forkhead box protein A1 ( FOXA1 ), potassium voltage-gated channel subfamily C member 3 ( KCNC3 ) and caspase-8 ( CASP8 ) exhibited high degrees in the transcriptional regulatory networks. In addition, the methylation profiles of NPY, TNF, FOXA1, KCNC3 and CASP8 were confirmed by another dataset. In summary, the present study systematically analyzed the DNA methylation profile of GBM using bioinformatics approaches and identified several abnormally methylated genes, providing insight into the molecular mechanism underlying GBM.
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