Wang Liping, Shao Guoguang, Zhang Wenjie, Guo Xiping, Wang Chunguang, An Jihong, Zhong Guogan, Zhao Hua
Dept. of Thoracic & Cardiovascular Surgery, Second Clinical College, Jilin University, Changchun 130041, China.
Zhonghua Zhong Liu Za Zhi. 2002 May;24(3):230-3.
To study the inhibition of voltage-activated K(+) conductance and cell proliferation by 4-aminopyridine (4-AP) in the human small-cell lung cancer (SCLC).
Inhibition of voltage-activated K(+) current by 4-AP through the whole-cell patch-clamp technique in SCLC cell line was studied. The influence on the cell-cycle by 4-AP was observed by flow cytometry to identify the in vitro inhibition by 4-AP to the cell proliferation of the SCLC cell line.
Exposure of the tumor cells to 5 mmol/L 4-AP reduced the peak outward K(+) current (evoked by a depolarization to +80 mV) from 1.22 +/- 0.11 nA (n = 30) to 0.59 +/- 0.10 nA (n = 28). Flow cytometry results showed that cell population accumulated in the G(0)/G(1) phase and a significantly reduced proportion in the S phase and G(1)/G(2) phase cells after having been exposed to 4-AP for three days. Incubation of the SCLC cells with 0.1, 5, 10, 15, 20 mmol/L 4-AP resulted in a concentration-and time-dependent reduction in the number of viable cells as compared with the control.
The voltage-activated K(+) channels expressed by SCLC play an important role in SCLC cell proliferation. The proliferation of the SCLC cells is inhibited by K(+) channel antagonists.
