Genetic inhibition of the atypical kinase Wee1 selectively drives apoptosis of p53 inactive tumor cells.

ABSTRACT:

Background

Tumorigenesis is the result of genomic or epigenomic insults and subsequent loss of the proper mechanisms to respond to these alterations leading to unscheduled growth. Tumors arising from these mutations often have altered cell cycles that offer proliferative advantages and lead to the accumulation of additional mutations that can lead to more aggressive phenotypes. Nevertheless, tumor cells must still adhere to the basic tenets of the cell cycle program to ensure their survival by DNA duplication, chromosomal segregation and cytokinesis. The atypical tyrosine kinase Wee1 plays a key role in regulating the cell cycle at the DNA synthesis and mitotic checkpoints via phosphorylation and subsequent inactivation of cyclin-dependent kinases (CDKs) in both healthy and tumorig

SUBMITTER: Pappano WN 

PROVIDER: S-EPMC4229861 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature