Abstract

[This corrects the article DOI: 10.18632/oncotarget.21109.].

Highlights

  • Over the past few decades, adenocarcinoma of the esophagogastric junction (AEG) has markedly increased in Western and Eastern countries [1,2,3,4,5]

  • C-terminal tensin-like (CTEN) plays a crucial role in tumor cell proliferation, migration, and invasion through its overexpression, which highlights its usefulness as a prognosticator and potential therapeutic target in AEG

  • Quantitative RT-PCR analysis was performed to test whether CTEN was overexpressed in gastric cancer cell lines compared with the normal organs (Figure 1A)

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Summary

Introduction

Over the past few decades, adenocarcinoma of the esophagogastric junction (AEG) has markedly increased in Western and Eastern countries [1,2,3,4,5]. Despite the improvement of diagnosis and treatment technologies over the past three decades such as extended radical resection and chemo and/or chemoradiotherapy, many AEG patients frequently develop metastasis and experience recurrence, and the long-term survival remains poor because of the aggressive and systemic nature of this disease [6]. Numerous genes have been analyzed to understand the molecular mechanisms of carcinogenesis and improve the clinical outcomes for adenocarcinoma of the esophagus and esophagogastric junction. To detect a novel treatment target for adenocarcinoma of the esophagogastric junction (AEG), we tested whether C-terminal tensin-like (CTEN), a member of the tensin gene family and frequently overexpressed in various cancers, acts as a cancer-promoting gene through overexpression in AEG

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