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Gastroenterology Research and Practice
Volume 2014 (2014), Article ID 185035, 8 pages
Research Article

Overexpression of FOXO3, MYD88, and GAPDH Identified by Suppression Subtractive Hybridization in Esophageal Cancer Is Associated with Autophagy

1Department of Pharmaceutical Biotechnology and Pharmaceutical Biotechnology Research Center, School of Pharmacy, Tehran University of Medical Sciences, Tehran 1417614411, Iran
2Pharmaceutical Sciences Research Center, Sari School of Pharmacy, Mazandaran University of Medical Sciences, Sari 48175-861, Iran
3Golestan Research Center of Gastroenterology and Hepatology, Golestan University of Medical Sciences, Golestan 49186-619, Iran
4Department of General Surgery, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran 19857-17443, Iran

Received 30 September 2013; Revised 12 December 2013; Accepted 16 December 2013; Published 8 January 2014

Academic Editor: D. Fan

Copyright © 2014 Mohammad Soltany-Rezaee-Rad et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To find genes involved in tumorigenesis and the development of esophageal cancer, the suppression subtractive hybridization (SSH) method was used to identify genes that are overexpressed in esophageal cancer tissues compared to normal esophageal tissues. In our SSH library, the forkhead box O3 (FOXO3), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and myeloid differentiation primary response 88 (MYD88) genes were the most highly upregulated genes, and they were selected for further studies because of their potential role in the induction of autophagy. Upregulation of these genes was also observed in clinical samples using qRT-PCR. In addition, coexpression analysis of the autophagy-related genes Beclin1, ATG12, Gabarapl, PIK3C3, and LC3 demonstrated a significant correlation between the differentially overexpressed genes and autophagy. Autophagy is an important mechanism in tumorigenesis and the development of chemoresistance in cancer cells. The upregulation of FOXO3, GAPDH, and MYD88 variants in esophageal cancer suggests a role for autophagy and provides new insight into the biology of esophageal cancer. We propose that FOXO3, GAPDH, and MYD88 are novel targets for combating autophagy in esophageal cancer.