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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Functional and molecular identification of intermediate-conductance Ca²⁺-activated K⁺ channels in breast cancer cells: association with cell cycle progression

¹Laboratoire de Physiologie Cellulaire, Institut National de la Santé et de la Recherche Médicale EMI 0228, SN3, Université des Sciences et Technologies de Lille, 59655 Villeneuve d'Ascq Cédex; ²Laboratoire de Physiologie Cellulaire et Moléculaire, Université Picardie Jules Verne, Faculté des Sciences, 80000 Amiens; ⁴Institut Fédératif de Recherche IFR22: "Biologie et Pathologie des Régulations Cellulaires," IRCL, 59045 Lille Cédex, France; and ³Laboratoire de Physiologie Animale, Université Ibnou Zohr, Faculté des Sciences, Agadir, Morocco BP2815 80000

Submitted 5 November 2003 ; accepted in final form 20 February 2004

We have previously reported that the hEAG K⁺ channels are responsible for the potential membrane hyperpolarization that induces human breast cancer cell progression into the G1 phase of the cell cycle. In the present study, we evaluate the role and functional expression of the intermediate-conductance Ca²⁺-activated K⁺ channel, hIK1-like, in controlling cell cycle progression. Our results demonstrate that hIK1 current density increased in cells synchronized at the end of the G1 or S phase compared with those in the early G1 phase. This increased current density paralleled the enhancement in hIK1 mRNA levels and the highly negative membrane potential. Furthermore, in cells synchronized at the end of G1 or S phases, basal cytosolic Ca²⁺ concentration ([Ca²⁺]_i) was also higher than in cells arrested in early G1. Blocking hIK1 channels with a specific blocker, clotrimazole, induced both membrane potential depolarization and a decrease in the [Ca²⁺]_i in cells arrested at the end of G1 and S phases but not in cells arrested early in the G1 phase. Blocking hIK1 with clotrimazole also induced cell proliferation inhibition but to a lesser degree than blocking hEAG with astemizole. The two drugs were essentially additive, inhibiting MCF-7 cell proliferation by 82% and arresting >90% of cells in the G1 phase. Thus, although the progression of MCF-7 cells through the early G1 phase is dependent on the activation of hEAG K⁺ channels, when it comes to G1 and checkpoint G1/S transition, the membrane potential appears to be primarily dependent on the hIK1-activity level.

breast cancer; calcium-activated potassium channels; proliferation

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