Notch1 induces cell cycle arrest and apoptosis in human cervical cancer cells: involvement of nuclear factor kappa B inhibition.

摘要: Notch signaling can serve as a tumor suppressor or promoter in the same kind of cancer, such human papillomavirus–positive cervical cancer cells. However, exact mechanisms remain poorly characterized. Our studies demonstrated that constitutively overexpressed active Notch1 via stable transfection with exogenous intracellular domain (ICN) resulted growth inhibition cell line HeLa by inducing G2–M arrest and apoptosis. Moreover, was correlated nuclear factor kappa B (NF-κB) p50 activation, accompanied decrease expression NF-κB an increase cytosolic IκBα. Consistent these results, downregulation cyclin D1 Bcl-2, which are both downstream genes NF-κB, were observed ICN-overexpressed Overall, our results suggest may contribute partially to cycle apoptosis induced activation