Abstract
BackgroundSnail1 is a transcription regulator of E-cadherin. The loss of E-cadherin seems to be a crucial step in the process of Epithelial-mesenchymal transition (EMT). EMT initiates invasion and proliferation in many tumours. Overexpression of Snail1 is known to be associated with poor outcome in several solid tumours. The aim of this study was to analyse its expression profile and prognostic significance in colorectal cancer.MethodsTissue microarrays (TMA) containing paraffin-embedded primary colorectal cancer (CRC) tissue samples from 251 patients were used in this study. The expression of Snail1 and E-cadherin was assessed by immunohistochemistry in different tumour compartments, corresponding lymph node metastases and normal colonic mucosa. Intensity of staining was classified according to the Remmele score (standardized scoring system) as well as the semiquantitative score established by Blechschmidt et al.ResultsSnail1 expression was observed in 76% of the CRC. Loss of E-cadherin was noted in 87% of the CRC. Snail1 positive tumours were significantly correlated with Snail1 positive lymph node metastases (p=0.03). There was no significant correlation between loss of E-cadherin and Snail1 expression, or between N-stage or grading and Snail1 expression. Kaplan-Meier survival analysis identified no prognostic impact of Snail1 expression on overall survival.ConclusionSnail1 expression was detectable in most of the CRC but showed no significant association with E-cadherin loss, clinical pathological characteristics or overall survival. The observed loss of E-cadherin could be explained by effects of other important EMT pathways, such as the Wnt-signalling cascade.
Highlights
Snail1 is a transcription regulator of E-cadherin
Snail1 expression and its association with E-cadherin in colorectal cancer We detected Snail1 in 76% (191/251) of the 251 samples, while E-cadherin expression was lacking in 39% (97/250) (Remmele score, Figure 1)
We detected no significant difference in the distribution of E-cadherin in the different tumour compartments and expression of Snail1 in the same compartment
Summary
The loss of E-cadherin seems to be a crucial step in the process of Epithelial-mesenchymal transition (EMT). Snail was the first characterized repressor of the invasion suppressor gene CDH1, which encodes for the crucial adhesion protein E-cadherin [1,2]. Loss of its expression or function diminishes cell–cell contacts and is known to be a key step during the process of Epithelial-mesenchymal transition (EMT). EMT describes it accompanies the invasiveness and metastatic behaviour of malignant cells [6,7]. Besides their involvement in EMT, Snail family members are involved in a variety of other processes, such as apoptosis or mesoderm formation in the developing embryo. The mechanism by which Snail influences these different cellular processes is still not totally understood
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