CDK1 Dysregulation in Breast Cancer

During the synthesis of DNA and chromosomal segregation, the checkpoints monitor the proper progression through the cell cycle and sense any defects. Via the modulation of CDK activity, these activated checkpoints lead to cell cycle arrest. However, any dysregulation in these kinases will impede this characteristic modulation during the cell cycle. Specific complexes of CDK-cyclins are deregulated frequently by mutations associated with tumors, and either unscheduled cell cycle re-entry or continuous proliferation is witnessed due to this deregulation. Furthermore, these two features are seen in most human tumor cells. The CDK1, along with its interacting partners (A and B cyclins), controls progression at the S-G2 and G2-M phases of the cell cycle. The CDK1 shows high expression in multiple cancers including breast cancer. The dysregulation of CDK1 could lead to many possible events, including enhanced tumor growth, increased cancer cell proliferation, and chromosomal instability. Multiple studies have demonstrated that the CDK1 expression levels and function are dysregulated, thus highlighting its participation in the BC progression. It has been witnessed that blocking or silencing the CDK1 could suppress the BC growth, particularly when combined with other anti-cancer agents. Many pan-CDK inhibitors targeting multiple CDKs including CDK1 have been tested at different phases of clinical trials. This chapter highlights the significant role of CDK1, its dysregulation in breast cancer, and the potential treatment available to combat the same.