Dinamics of Kv10.1 expression through the cell cycle of cancer and non-cancer cells

摘要: Kv10.1 is a voltage dependent potassium channel. Its expression has been reported to be widespread in clinical tumors samples of diverse origin. In contrast, normal non-neural tissue detected at low levels, and only restricted populations cells (Hemmerlein, Weseloh et al. 2006). shown associated with poor survival, channel also appears increased upon mitogen factor stimulation (Borowiec, Hague 2007), favors cell proliferation, tumor progression (Pardo, del Camino 1999, Weber, Mello de Queiroz 2006, Downie, Sanchez 2008). It believed that expressing acquire selective advantages allow them maintain chronic proliferation. Through this study we identified dependency on cycle, possible mechanism underlying cancer cells. expressed defined, narrow time window during G2/M. The Rb/E2F1 pathway regulates its course. complex represses transcription Kv10.1, the disruption by HPV-E7 leads release E2F1 factor, which directly binds Kv10.1pr activate transcription. Furthermore, show asynchronous HeLa cells, knockdown increases G2/M fraction, suggesting absence spend, average, more Finally, taking into account kinetics, found non-neuronal tissue. A proliferating population located bottom sides colonic crypts positive for Kv10.1. These findings can help mechanistically explain influence proliferation aberrant tumors. results reinforce idea as switch participates regulation, assembly disassembly primary cilium, therefore controls exit entrance cycle.