Abstract
Ezrin is involves in multiple cancer cell functions. In this study, differentially expressed genes (DEGs) identified from mRNA expression profiling following Ezrin knockdown in esophageal squamous cell carcinoma (ESCC), were analyzed by multiple bioinformatics methods for a comprehensive understanding. Gene Ontology enrichment found significant terms related to immunity, stimulus response, extracellular matrix-binding and signal transduction. Functional Annotation Chart showed except GO categories, these DEGs were annotated by 72 functional category terms. Subpathway analyses revealed the DEGs were involved in 36 subpathways, overwhelming the traditional pathway enrichment. Promoter analyses showed specific sequence patterns and transcription factors correspond to the co-downregulation and co-upregulation of DEGs. MNB1A, DOF2, PBF, YY1, PRRX2, UBX and ARNTAHR co-regulate the downregulated genes, whereas GATA2, ZNF42, deltaEF1, MYCN and ARNT co-regulate the upregulated genes. This paper provides a workflow for a better understanding the roles of Ezrin knockdown in ESCC by the bioinformatics analyses of its DEGs.
Highlights
Ezrin, named VIL2, is a member of the Ezrin–radixin– moesin (ERM) protein family
Our previous researches show Ezrin is over-expressed in human esophageal squamous cell carcinoma (ESCC), which is associated with the invasive phenotype of malignantly transformed esophageal epithelial cells [8]
We subsequently found Ezrin translocates from the plasma membrane to the cytoplasm in the progression from normal epithelium to invasive carcinoma of esophageal epithelial cells [9]
Summary
Named VIL2, is a member of the Ezrin–radixin– moesin (ERM) protein family. Ezrin acts as a linker between the actin cytoskeleton and plasma membrane proteins, as well as a signal transducer involving in cytoskeletal remodeling [1]. Ezrin has been implicated in multiple aspects of cancer cell function, especially the metastasis of cancer cells [2,3,4]. Ezrin translocates to the nucleus to regulate gene transcription in several cancer cell types [57]. Our previous researches show Ezrin is over-expressed in human esophageal squamous cell carcinoma (ESCC), which is associated with the invasive phenotype of malignantly transformed esophageal epithelial cells [8]. We subsequently found Ezrin translocates from the plasma membrane to the cytoplasm in the progression from normal epithelium to invasive carcinoma of esophageal epithelial cells [9]
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