Evaluation of the Correlativity of Gender Determining Region Y-box 4, N-cadherin, CD44 and E-cadherin Expression in the Prognosis of Esophageal Squamous Cell Carcinoma

Overview

Journal Int J Clin Exp Pathol

Specialty Pathology

Date 2020 Jan 15

PMID 31933993

Citations 1

Authors

Yanzi Qin

Wenjun Zhao

Lili Cheng

Jin Gao

Zhaonan Bian

Shiwu Wu

Zenong Cheng

Yisheng Tao

Li Ma

Affiliations

Soon will be listed here.

Abstract

Background: SOX4 is highly expressed in many different tumor types, and SOX4 has been reported in the literature to participate in tumor proliferation, damaging and movement by leading Epithelial-Mesenchymal Transition. Cancer vital cells and Epithelial-Mesenchymal Transition have been repeatedly confirmed to participate during the proliferation, damaging and movement of cancer. This research examined the association of the Epithelial-Mesenchymal Transition-related molecules E-cadherin, N-cadherin, CD44, and SOX4 in the ESCC and aimed for providing inspiration for clinical treatment as well as to indicate a new direction for detecting invasion and forecasting the prospect of affected role using ESCC.

Methods: Immunohistochemistry was utilized to observe the expression of the S0X4, N-cadherin, CD44 and E-cadherin proteins. Survival analysis of the positive and negative SOX4, E-cadherin, N-cadherin and CD44 protein expression groups was performed by the Kaplan-Meier approach.

Outcomes: A confirming relationship was observed among the expression of SOX4, N-cadherin or CD44 and tumor diameter, distant metastasis, deepness of damaging, lymph node metastasis, pTNM stage and histological grade (<0.05). Spearman correlativity calculation displayed that the expression of the SOX4 protein was obviously responded with the expression of the N-cadherin and CD44 proteins. Moreover, the expression of the N-cadherin and CD44 proteins was also positively correlated. The E-cadherin protein was negatively correlated with SOX4, N-cadherin and CD44 protein expression in ESCC. SOX4, N-cadherin, CD44, E-cadherin, age and distant metastasis were determined to be separate elements that influenced the prognosis of patients with ESCC.

Conclusions: We found that suppression of ESCC providers can suppress the growth of bad tumors and change therapeutic results for ESCC patient since CD44 supports the induction of Epithelial-Mesenchymal Transition in ESCC.

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