Affiliations: [a] Division Of Cancer Research, Regional Cancer Centre, Medical College. P.O, Trivandrum- 695 011, Kerala, India. Tel.: +91 0471 522203; Fax: +91 0471 447454; E-mail: smritimk@hotmail.com | [b] Department of Cytopathology, Regional Cancer Centre, Medical College. P.O, Trivandrum- 695 011, Kerala, India | [c] Division of Cancer Research, Regional Cancer Centre, Trivandrum 695 011, Kerala, India. Tel.: +91 0471 522203; Fax: +91 0471 447454; E-mail: prabhabalaram@yahoo.co.in
Correspondence:
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Corresponding author: Dr. Smriti. M. Krishna, M.Phil., Department of Medical Microbiology, Faculty of Medicine & Health Sciences, U.A.E. University, AL AIN, U. A. E India. Tel.: +971 50 5088699; Fax: +971 03 7671966; E-mail: smritimk@hotmail.com.
Abstract: Nasopharyngeal carcinoma (NPC) is a unique tumour due to its aetiology, incidence pattern and its consistent association with Epstein-Barr virus (EBV). EBV encodes many viral proteins, which targets crucial cell cycle regulatory proteins. Cadherins are a family of transmembrane glycoproteins, which mediates Ca2+-dependent intercellular adhesion. Epithelial (E)-cadherin is an important member of this family, which is expressed predominantly on the surface of epithelial cells. E-cadherin acts as an invasion/metastasis-suppressor gene, hence knowledge of the molecular mechanism that controls its expression or function is of primary importance in understanding the process of tumor invasion. Loss of E-cadherin function has been shown to potentiate tumor cell invasion and interestingly, a large number of invasive tumors do not involve mutation of E-cadherin, but rather down regulation of expression. Hence in this study, an attempt was made to evaluate the protein level expression pattern of E-cadherin in relation to viral involvement and to correlate it with other clinico-pathological parameters. We observed a significant down regulation of E-cadherin in NPC and its histological subsets, when compared to the controls (p ‹ 0.001). Expression of E-cadherin ranged from mild to moderate and none of the NPC showed intense expression. E-cadherin expression showed a significant down-regulation in NPC lesions with EBV infection (r=−0.436, p ‹ 0.001). The down regulation of E-cadherin observed in NPC is in line with the previous reports in E-cadherin expression in various cancers. The total lack of E-cadherin expression in neoplastic cells might be due to hypermethylation of E-cadherin promoter or its down regulation by cellular transcription repressor. Our study also shows a significant down regulation of E-cadherin in the presence of EBV, which also might involve the cellular DNA methylation machinery.
