Immunohistochemical Expression of E-Cadherin in Canine Oral Melanoma
World Small Animal Veterinary Association World Congress Proceedings, 2015
S. Pisamai1; A. Runsipipat2; C. Kulprawit3; G. Suriyaphol1
1Biochemistry Unit Department of Veterinary Physiology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand; 2Department of Veterinary Pathology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand; 3Department of Veterinary Surgery, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand

Introduction

Canine oral melanoma (cOM) is the most oral malignancy in dogs because of the metastatic behavior of cancer cells. According to the TNM staging system, stage III criteria include a tumor more than 4 cm in diameter or involvement of regional lymph node metastasis. Cell adhesion molecules, including E-cadherin, play pivotal roles in cancer invasion and metastasis. Loss of E-cadherin function was described in migrating cancer cells due to the suppression of cell-cell-adhesion in the epithelial-mesenchymal transition (EMT) process and loss of antigrowth signals.

Objective

To investigate E-cadherin expression in cOM by immunohistochemistry (IHC).

Methods

E-cadherin expression in stage III melanotic and amelanotic cOM (n = 7) and normal canine gingival tissues (n = 7) was evaluated by IHC. The anti-E-cadherin antibody (mouse monoclonal, clone 36, BD Biosciences) at dilution of 1:100 was used. The average percentage of positive staining areas was compared between cOM and normal tissues. Statistical difference was performed by Mann-Whitney test.

Results

The IHC results showed that E-cadherin expression significantly decreased in cOM (16.44% ± 8.051) compared to normal tissues (61.24% ± 8.994) (p < 0.01) (Figure 1).

Figure 1
Figure 1

Immunohistochemical staining for E-cadherin in normal gingiva (A) and cOM (B) (scale bars = 20 µm).
 

Conclusion

In summary, these results suggested that loss of E-cadherin has been associated with cOM progression by providing cancer cells to activate invasion and metastasis.

Acknowledgement

Ratchadaphiseksomphot Endowment Fund (grant number R_017_2556), Chulalongkorn University graduate scholarship to commemorate the 72nd anniversary of His Majesty King Bhumibol Adulyadej and Doctoral Degree Chulalongkorn University 100th year birthday anniversary scholarship.

  

Speaker Information
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G. Suriyaphol
Biochemistry Unit Department of Veterinary Physiology
Faculty of Veterinary Science
Chulalongkorn University
Bangkok, Thailand


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