Overexpression of human β-defensin 2 promotes growth and invasion during esophageal carcinogenesis
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1 Division of Medical Oncology, Department of Internal Medicine, The Ohio State University, Columbus, Ohio
2 Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University, Columbus, Ohio
3 Center for Biostatistics, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Columbus, Ohio
Dr. Tong Chen, M.D. Ph.D., e-mail: email@example.com
Key Words: Human β-defensin 2, esophageal squamous cell carcinoma and carcinogenesis
Received: July 07, 2014 Accepted: August 28, 2014 Published: September 05, 2014
Human β-defensin 2 (HBD-2) is an antimicrobial peptide produced by mucosal surfaces in response to microbial exposure or inflammatory cytokines. Although HBD-2 is expressed in the esophagus in response to stress and infectious agents, little is known regarding its expression and functional role in esophageal carcinogenesis. In the current investigation, normal esophagus and N-nitrosomethylbenzylamine (NMBA)-induced precancerous and papillomatous lesions of the rat esophagus were characterized for HBD-2 encoding gene Defb4 and protein. HBD-2 was found to be overexpressed in esophagi of rats treated with NMBA compared to animals in control group. Results of Real-time PCR, Western blot and immunohistochemistry demonstrated a positive correlation between the overexpression of HBD-2 and the progression of rat squamous cell carcinogenesis (SCC) in the esophagus. We also observed that HBD-2 is overexpressed in tumor tissues removed from patients with esophageal SCC. Moreover, Defb4 silencing in vitro suppresses the tumor cell proliferation, mobility and invasion in esophageal SCC cell line KYSE-150. The results from this study provide experimental evidence that HBD-2 may play an oncogenic role in the initiation and progression of esophageal SCC and thus serves as a target for chemopreventive and therapeutic interventions.
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