Association of E-cadherin & vimentin expression with clinicopathological parameters in lingual squamous cell carcinomas & their role in incomplete epithelial mesenchymal transition

Abstract

Background & objectives: Lingual squamous cell carcinomas (SCC) pose a major public health burden in India. Epithelial-mesenchymal transition (EMT) is the conversion of an epithelial cell to a mesenchymal phenotype at the invasive front (IF) enhancing invasiveness of these cells which may be studied using immunohistochemistry. The objective of this study was to assess the expression of E-cadherin and vimentin at the IF, and their correlation with the histological risk assessment score, clinicopathological parameters and lymph node metastasis. Methods: Thirty consecutive untreated patients diagnosed as lingual SCC who underwent hemiglossectomy over one year formed the study group. The immunohistochemical expression of E-cadherin and vimentin in the periphery as well as the centre of tumour islands was correlated with clinicopathological parameters, Brandwein-Gensler risk assessment score and lymph node metastasis, along with a correlation between the coexpression of two markers at the IF. Results: Loss of E-cadherin expression was seen at IF in 83.3 per cent (25/30) cases. Out of these, 20 per cent (5/25) showed a corresponding gain in vimentin expression (complete epithelial-mesenchymal transition) and 80 per cent (20/25) did not. Overall, 16.6 per cent (5/30) cases showed complete EMT. However, no correlation between E- cadherin and vimentin expression at the IF was found. No statistical significance was found between E-cadherin loss and vimentin gain at the IF, with the various parameters or the risk score. Interpretation & conclusions: The present study suggests that the cells at IF may metastasize even without a gain in vimentin expression (without classical EMT), as cohesive clusters showing incomplete EMT (E-cadh-/Vim-).

Targeting of H19/cell adhesion molecules circuitry by GSK-J4 epidrug inhibits metastatic progression in prostate cancer

“…From a molecular point of view, H19 acts as a transcriptional repressor of cell adhesion molecules by increasing the H3K27me3 level at the corresponding promoter regions. Upon H19 reduction, transcription of CDH1 and ITGB4 is released, increasing metastatic potential, and metastasis dissemination through a mechanism also known as “cohesive metastatic phenotype” described for prostate cancer [ 24 , 29 ] as well as for other cancer types like colorectal cancer and squamous cell carcinomas as recently reported [ 48 , 49 ]. A cluster of tumoral cells, linked together by E-cadherin and capable of motility through β4 integrin expression and function, is present in lung parenchyma and lung vessels after injecting siH19 cells in the tail vein of NSG mice (Fig.…”