Cyclic expression of the voltage‐gated potassium channel K(V)10.1 promotes disassembly of the primary cilium

The primary cilium, critical for morphogenic and growth factor signaling, is assembled upon cell cycle exit, but the links between ciliogenesis and cell cycle progression are unclear. K(V)10.1 is a voltage‐gated potassium channel frequently overexpressed in tumors. We have previously reported that expression of K(V)10.1 is temporally restricted to a time period immediately prior to mitosis in healthy cells. Here, we provide microscopical and biochemical evidence that K(V)10.1 localizes to the centrosome and the primary cilium and promotes ciliary disassembly. Interference with K(V)10.1 ciliary localization abolishes not only the effects on ciliary disassembly, but also K(V)10.1‐induced tumor progression in vivo. Conversely, upon knockdown of K(V)10.1, ciliary disassembly is impaired, proliferation is delayed, and proliferating cells show prominent primary cilia. Thus, modulation of ciliogenesis by K(V)10.1 can explain the influence of K(V)10.1 expression on the proliferation of normal cells and is likely to be a major mechanism underlying its tumorigenic effects.