The involvement of Kv3.4 voltage-gated potassium channel in the growth of an oral squamous cell carcinoma cell line

被引:17
作者
Lew, TS
Chang, CS
Fang, KP
Chen, CY
Chen, CH
Lin, SC
机构
[1] Natl Yang Ming Univ, Sch Dent, Inst Oral Biol, Taipei 112, Taiwan
[2] Natl Yang Ming Univ, Inst Physiol, Taipei 112, Taiwan
[3] Vet Gen Hosp Taipei, Dept Dent, Taipei, Taiwan
关键词
K(v)3.4; mouth; neoplasm; oral carcinoma; potassium channel;
D O I
10.1111/j.1600-0714.2004.00236.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
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-! 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-! 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-! 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.
引用
收藏
页码:543 / 549
页数:7
相关论文
共 25 条
[11]   Cloned potassium channels from eukaryotes and prokaryotes [J].
Jan, LY ;
Jan, YN .
ANNUAL REVIEW OF NEUROSCIENCE, 1997, 20 :91-123
[12]  
KEYOMARSI K, 1991, CANCER RES, V51, P3602
[13]   Regulation of IGFBP-5 expression during tumourigenesis and differentiation of oral keratinocytes [J].
Lin, SC ;
Wang, CP ;
Chen, YM ;
Lu, SY ;
Fann, MJ ;
Liu, CJ ;
Kao, SY ;
Chang, KW .
JOURNAL OF PATHOLOGY, 2002, 198 (03) :317-325
[14]  
LO KY, 1982, CANCER RES, V42, P2644
[15]   POTASSIUM CHANNELS AND REGULATION OF PROLIFERATION OF HUMAN-MELANOMA CELLS [J].
NILIUS, B ;
WOHLRAB, W .
JOURNAL OF PHYSIOLOGY-LONDON, 1992, 445 :537-548
[16]  
PANCRAZIO JJ, 1993, ANTICANCER RES, V13, P1231
[17]   Oncogenic potential of EAG K+ channels [J].
Pardo, LA ;
del Camino, D ;
Sánchez, A ;
Alves, F ;
Brüggemann, A ;
Beckh, S ;
Stühmer, W .
EMBO JOURNAL, 1999, 18 (20) :5540-5547
[18]   PROFOUND DIFFERENCES IN POTASSIUM CURRENT PROPERTIES OF NORMAL AND ROUS-SARCOMA VIRUS-TRANSFORMED CHICKEN-EMBRYO FIBROBLASTS [J].
REPP, H ;
DRAHEIM, H ;
RULAND, J ;
SEIDEL, G ;
BEISE, J ;
PRESEK, P ;
DREYER, F .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (08) :3403-3407
[19]   CLONING OF A HUMAN CDNA EXPRESSING A HIGH VOLTAGE-ACTIVATING, TEA-SENSITIVE, TYPE-A K+ CHANNEL WHICH MAPS TO CHROMOSOME-1 BAND-P21 [J].
RUDY, B ;
SEN, K ;
VEGA-SAENZ DE MIERA, E ;
LAU, D ;
RIED, T ;
WARD, DC .
JOURNAL OF NEUROSCIENCE RESEARCH, 1991, 29 (03) :401-412
[20]   Functional up-regulation of HERG K+ channels in neoplastic hematopoietic cells [J].
Smith, GAM ;
Tsui, HW ;
Newell, EW ;
Jiang, XP ;
Zhu, XP ;
Tsui, FWL ;
Schlichter, LC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (21) :18528-18534