IADR Abstract Archives
Characterization of Cx43 and Epithelial-Mesenchymal Transition Proteins in Oral Cancer
Objectives: The epithelial-mesenchymal transition (EMT) is a process of transcriptional reprogramming of epithelial cells with a crucial role in early events, such as oncogenesis and invasion, and late events, such as migration and metastasis. The hallmark is the alteration of the expression of adhesion molecules (downregulation of E-cadherin and upregulation of N-cadherin), which is regulated by complex signaling pathways, not entirely known, and understood. Cx43 is a gap junction protein, responsible for the communication of neighboring cells, but its role in EMT of oral cancer is poorly understood.
For this reason, we studied the immunohistochemical expression of the Cx43 in paraffin-embedded primary and metastatic tumors. Posteriorly, the Cx43, E-cadherin, and N-cadherin expression was measured in normal or keratinocytes (NOK) and cancer cell lines (SCC9 and SCC25).
Methods: Five non-metastatic primary tumors, five metastatic primary tumors, and their lymph nodes were stained for fluorescent immunohistochemistry. DAPI was used for nuclei and CD45 for lymphocytes.
After this, cell lines from primary tongue cancer (SCC9 and SCC25) and one primary cell line from normal oral keratinocytes (NOK) were studied. The expression of Cx43, E-cadherin, and N-cadherin was measured by western blot and immunocytochemistry.
Results: The expression of Cx43 was higher in non-metastatic primary tumors when compared with metastatic primary tumors. Surprisingly, a well-defined net of Cx43 was evidenced in lymph nodes.
In cell lines, a correlation in the expression of Cx43 and E-cadherin in NOK was observed, but disorganization of connexin expression in cancer cell lines is associated with the upregulation of N-cadherin. In these cells, a previously not reported expression of Cx43 in the nuclei was observed.
Conclusions: These findings demonstrate that the E-Cadherin and N-Cadherin switch observed in the EMT of oral cancer cells also affects the expression of Cx43. Based on the results, we suggest that a probable translocation of Cx43 to the nucleus can play a role in the regulation of the adhesion molecules switch in the EMT of oral squamous cell carcinoma.
For this reason, we studied the immunohistochemical expression of the Cx43 in paraffin-embedded primary and metastatic tumors. Posteriorly, the Cx43, E-cadherin, and N-cadherin expression was measured in normal or keratinocytes (NOK) and cancer cell lines (SCC9 and SCC25).
Methods: Five non-metastatic primary tumors, five metastatic primary tumors, and their lymph nodes were stained for fluorescent immunohistochemistry. DAPI was used for nuclei and CD45 for lymphocytes.
After this, cell lines from primary tongue cancer (SCC9 and SCC25) and one primary cell line from normal oral keratinocytes (NOK) were studied. The expression of Cx43, E-cadherin, and N-cadherin was measured by western blot and immunocytochemistry.
Results: The expression of Cx43 was higher in non-metastatic primary tumors when compared with metastatic primary tumors. Surprisingly, a well-defined net of Cx43 was evidenced in lymph nodes.
In cell lines, a correlation in the expression of Cx43 and E-cadherin in NOK was observed, but disorganization of connexin expression in cancer cell lines is associated with the upregulation of N-cadherin. In these cells, a previously not reported expression of Cx43 in the nuclei was observed.
Conclusions: These findings demonstrate that the E-Cadherin and N-Cadherin switch observed in the EMT of oral cancer cells also affects the expression of Cx43. Based on the results, we suggest that a probable translocation of Cx43 to the nucleus can play a role in the regulation of the adhesion molecules switch in the EMT of oral squamous cell carcinoma.