Identification of Distinct Gene Expression Profiles between Esophageal Squamous Cell Carcinoma and Adjacent Normal Epithelial Tissues

• Published in: The Tohoku Journal of Experimental Medicine Vol. 226; no. 4; pp. 301 - 311
• Main Authors: Tao, Yisheng, Chai, Damin, Ma, Li, Zhang, Ting, Feng, Zhenzhong, Cheng, Zenong, Wu, Shiwu, Qin, Yanzi, Lai, Maode
• Format: Journal Article
• Language: English
• Published: Japan Tohoku University Medical Press 2012
• Subjects: Aged; Carcinoma, Squamous Cell - genetics; Carcinoma, Squamous Cell - pathology; cDNA microarray; Child; Epithelium - physiology; Esophageal Neoplasms - genetics; Esophageal Neoplasms - pathology; esophageal squamous cell carcinoma; Esophagus - cytology; Esophagus - physiology; gene expression; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Humans; immunohistochemistry; Middle Aged; Mucous Membrane - physiology; normal epithelial tissue; Oligonucleotide Array Sequence Analysis
• ISSN: 0040-8727; 1349-3329
• DOI: 10.1620/tjem.226.301

Esophageal squamous cell carcinoma (ESCC) is a predominant type of esophageal cancer, which is a malignant tumor originating from the esophageal mucosa or gland and is aggressive with poor prognosis. Identification of new gene expression patterns would be helpful for providing new targets for the early detection and treatment of ESCC patients. In the present study, we employed cDNA array technology to compare gene expression profiles between ESCC tissues and adjacent normal epithelial tissues from ESCC patients. There was at least a 4-fold change in the expression levels of 72 genes that were significantly increased and 107 genes that were decreased in ESCC compared with normal esophageal epithelium. Among them, genes known to be involved in ESCC were found, including matrix metalloproteinases, transcription factors SOX-4 and SOX-17, the Wingless-type MMTV integration site family member 2, and cell cycle regulators. Moreover, we have newly identified the two genes that are down-regulated in ESCC: monoamine oxidase A, an enzyme that catalyzes monoamines oxidation and 15-hydroxyprostaglandin dehydrogenase [NAD+], a prostaglandin-synthesizing enzyme that physiologically antagonizes COX-2. Likewise, we found the three genes that are up-regulated in ESCC: CD7, a cell surface glycoprotein member of the immunoglobulin superfamily, LIM-domain kinase 1, a small subfamily with an unique combination of two N-terminal LIM motifs and a C-terminal protein kinase domain, and TTK protein kinase, a previously unidentified member of the kinase family. These newly identified genes may be involved in the progression of the tumor and/or represent properties specific to ESCC.