BACKGROUND: In our previous study, an A-type voltage-gated K(+) channel, K(v)3.4, was found more frequently expressed in oral squamous cell carcinoma (OSCC) when compared with non-cancerous matched oral tissue. An OSCC cell line, OECM-1, was found to have moderate level of K(v)3.4 expression. METHODS: To further elucidate the roles of K(v)3.4 for the involvement of neoplastic process, we amplified K(v)3.4 coding sequence by reverse transcriptase polymerase chain reaction (RT-PCR), constructed an expression vector carrying this sequence and then stably transfected into OECM-1 OSCC cells. RESULTS: We demonstrated the integration and constitutive expression of K(v)3.4 in the cell. A unique A-type current elicited by such expression in OECM-1 cells was defined by patch clamp analysis. This current pattern can be reversibly blocked by an A-type K(+) channel blocker 2 mM 4-aminopyridine (4-AP). The acquisition of K(v)3.4 activity in OECM-1 cells bestowed growth advantage. However, in 3T3 cell, transfected K(v)3.4 caused only limited increase of growth without forming transformation foci. CONCLUSION: The present study established a stable keratinocyte system carrying functional K(v)3.4 and increase of growth, by which the anti-K(v)3.4 modalities for potential OSCC control can be further investigated.
BACKGROUND: In our previous study, an A-type voltage-gated K(+) channel, K(v)3.4, was found more frequently expressed in oral squamous cell carcinoma (OSCC) when compared with non-cancerous matched oral tissue. An OSCC cell line, OECM-1, was found to have moderate level of K(v)3.4 expression. METHODS: To further elucidate the roles of K(v)3.4 for the involvement of neoplastic process, we amplified K(v)3.4 coding sequence by reverse transcriptase polymerase chain reaction (RT-PCR), constructed an expression vector carrying this sequence and then stably transfected into OECM-1 OSCC cells. RESULTS: We demonstrated the integration and constitutive expression of K(v)3.4 in the cell. A unique A-type current elicited by such expression in OECM-1 cells was defined by patch clamp analysis. This current pattern can be reversibly blocked by an A-type K(+) channel blocker 2 mM 4-aminopyridine (4-AP). The acquisition of K(v)3.4 activity in OECM-1 cells bestowed growth advantage. However, in 3T3 cell, transfected K(v)3.4 caused only limited increase of growth without forming transformation foci. CONCLUSION: The present study established a stable keratinocyte system carrying functional K(v)3.4 and increase of growth, by which the anti-K(v)3.4 modalities for potential OSCC control can be further investigated.