Figure 7. Schematic diagram of a proposed interplay between CHEK1 and IKKε in OC cells.

In ovarian cancer cells characterized with high genomic instability, intrinsic DNA damage is repaired by overexpressed CHEK1. Through a pathological balance between IKKε and CHEK1, G2 to M transition is either promoted or blocked depending on the level of intrinsic DNA damage to facilitate cellular proliferation and survival. Ovarian cancer cells expressing high levels of IKKε block apoptosis by maintaining the low level of p21 to support cellular survival. When IKKε and CHEK1 are inhibited, accumulated intrinsic DNA damage and increased level of p21 trigger cellular apoptosis.