It has been shown that death-associated protein kinase (DAPK) family and E-cadherin play significant roles in the promotion of apoptosis and the suppression of cell adhesion and migration, and are involved in tumor metastasis. Ezrin, a cytoplasmic peripheral membrane protein, has been shown to interact with E-cadherin to participate in the metastasis of tumor cells. The present study aimed to investigate the expression of DRP-1 (a member of the DAPK family), ezrin and E-cadherin in esophageal squamous cell carcinoma (ESCC), and to analyze their association with clinicopathological factors in order to explore their potential in ESCC diagnosis. The expression of these genes was studied in tissue microarrays using in situ hybridization and immunohistochemistry methods in 76 specimens of ESCC and their paracancerous normal squamous epithelium tissues. Expression was statistically analyzed with regard to clinicopathological factors using χ2 and non-parametric tests. The expression level of DRP-1 was significantly different between the ESCC and paracancerous tissues (P<0.05). The expression level was correlated with the depth of invasion and lymph node metastasis (P<0.05). Abnormal E-cadherin expression was found to be associated with a high degree of cancer differentiation and lymph node metastasis (P<0.05). A positive correlation was observed between the expression of DRP-1 and E-cadherin (P<0.05). The expression of ezrin was found to be correlated with the depth of ESCC invasion, the degree of differentiation and lymph node metastasis (P<0.05). The high expression of ezrin has been previously shown to be correlated with the low or absent expression of E-cadherin. In conclusion, in ESCC, the expression levels of DRP-1, ezrin and E-cadherin were all reduced, and this reduction or absence of expression may have been attributed to ESCC tumorigenesis and progression. Simultaneous analyses of DRP-1, ezrin and E-cadherin expression levels would be useful to determine the malignancy and metastatic potential of ESCC, and these genes are consequently of potential use as biomarkers for the diagnosis and prognosis assessment of early-stage ESCC.
The aim of this study was to investigate the expression levels of the death-associated protein kinase (DAPK) and E-cadherin in esophageal squamous cell carcinoma (ESCC) and their correlation with clinical and pathological factors. Immunohistochemistry [streptavidin-peroxidase (SP) method], in situ hybridization, immunoblot assays and reverse transcription-PCR (RT-PCR) were used to detect the expression of DAPK and E-cadherin in the carcinomas and the adjacent normal tissues of 76 cases of esophageal squamous carcinomas. The immunoblot assay indicated that the expression levels of DAPK and E-cadherin were decreased significantly in the ESCC tissue (P<0.05) when compared with the adjacent normal tissues. The RT-PCR results showed that the mRNA levels of DAPK and E-cadherin were reduced. The abnormal expression of DAPK was highly correlated with the invasiveness and lymphatic metastasis of the cancer. The abnormal expression of E-cadherin was highly correlated with the differentiation and lymphatic metastasis of the cancer. The decreased expression levels of DAPK and E-cadherin correlated with the development of ESCC. The combined detection of DAPK and E-cadherin proteins may be correlated with the degree of malignancy and metastatic potency of ESCC.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.