Cortactin overexpression in the esophageal squamous cell carcinoma and its involvement in the carcinogenesis

• Published in: Diseases of the esophagus 2008-08, Vol.21 (5), p.402-408
• Main Authors: Hsu, N. Y., Yeh, K. T., Chiang, I. P., Pai, L. Y., Chen, C. Y., Ho, H. C.
• Format: Article
• Language: English
• Subjects: Adult; Aged; Animals; arecoline; Biomarkers, Tumor - metabolism; Carcinoma, Squamous Cell - metabolism; Carcinoma, Squamous Cell - pathology; Case-Control Studies; Cohort Studies; cortactin; Cortactin - metabolism; Disease Models, Animal; Esophageal Neoplasms - metabolism; Esophageal Neoplasms - pathology; esophageal squamous cell carcinoma; Female; Gene Amplification; Humans; Male; Mice; Middle Aged; Neoplasm Invasiveness - pathology; Neoplasm Staging; Precancerous Conditions - metabolism; Precancerous Conditions - pathology; Prognosis; Risk Assessment; RNA, Messenger - analysis; Sensitivity and Specificity; Survival Analysis
• ISSN: 1120-8694; 1442-2050
• DOI: 10.1111/j.1442-2050.2007.00775.x

The aim of this study is to examine whether dysregulated expression of cortactin occurs in esophageal squamous cell carcinoma (ESCC) and is involved in the development of ESCCs. An immunohistochemistry study for cortactin expression was performed on 46 pairs of surgically resected non‐tumor and ESCC tumor tissues and murine tumors of esophagi induced by a carcinogen. The results show increased cortactin expression in 20 and in 22 to a lesser extent, out of a total 46 ESCC tumor tissues. Increased cortactin was also detected in the premalignant lesions, the early stage dysplasia and carcinoma in situ, of ESCC tumor tissues. Differential polymerase chain reaction results showed slight increases in the EMS1 gene only in two of 10 ESCC tumor tissues, suggesting that EMS1 gene amplification is not the only mechanism for cortactin overexpression. In the mouse model induced by treatment with 4‐nitroquinoline 1‐oxide and arecoline, increased cortactin was detected in the epithelia with hyperkeratosis, papillomas, and ESCCs with invasion into the submucosa, respectively. Overall, we observed cortactin overexpression in early and late stages of human ESCCs and carcinogen‐induced murine ESCCs, suggesting a role for cortactin in esophageal carcinogenesis.