Abstract:
:Aims Epithelial mesenchymal transition (EMT) is a crucial process for acquisition of malignant phenotype, aggressiveness, and metastatic capacity in neoplasms. It is characterized by loss of epithelial markers and gain of mesenchymal markers. Studies on EMT and its potential association with the histological grading are sparse in oral squamous cell carcinoma (OSCC). This study aims to evaluate the expression of EMT-associated proteins-E-cadherin, β-catenin, and N-cadherin-in different grades of OSCC. Methodology In all, 60 cases of OSCC further subdivided into 20 cases each of well-, moderately, and poorly differentiated OSCCs were stained immunohistochemically with E-cadherin, β-catenin, and N-cadherin antibodies. The differences in the expression were evaluated using χ2 and Fisher exact tests, whereas Spearman's correlation was used to analyze the correlation between the markers. Results A reduced E-cadherin expression noted in 40% of the OSCCs was associated with reduced β-catenin expression in 66.6% of the cases and increase in the expression of mesenchymal N-cadherin seen in 80% of cases. This expression pattern demonstrated a significant association with histological grades. A membrane to cytoplasmic shift of E-cadherin (73.3%) and β-catenin (78.3%) increased with histological grade. A negative correlation was observed with the E-cadherin and N-cadherin localization, though it did not reach statistical significance. Conclusion OSCC tissues had high levels of EMT phenotype as compared with the normal oral mucosa. This phenotype was characterized by reduced E-cadherin and β-catenin expression and overexpression of N-cadherin. Aberrant localization of the studied proteins was a hallmark for depicting EMT.
journal_name
Int J Surg Patholjournal_title
International journal of surgical pathologyauthors
Angadi PV,Patil PV,Angadi V,Mane D,Shekar S,Hallikerimath S,Kale AD,Kardesai SGdoi
10.1177/1066896916654763subject
Has Abstractpub_date
2016-12-01 00:00:00pages
696-703issue
8eissn
1066-8969issn
1940-2465pii
1066896916654763journal_volume
24pub_type
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