and were inefficiently repaired in control-treated MCF7 cells, which express high levels of Wip1, compared with Wip1 shRNA-treated cells, in which Wip1 was depleted (56). Therefore, accumulation of gamma-H2AX at DSBs is critical for cell cycle arrest and efficient DNA repair and overexpression of Wip1 inhibits both processes. Additionally, gamma-H2AX plays a role in tumorigenesis (58), and a role for Wip1 in removal of gamma-H2AX after oncogenic stress and in the absence of DNA damage will be discussed below in section 4.5.
