When this gene becomes mutated, the protein becomes stable
and abundant accumulating in the nucleus of cells thereby causing cancer. This
has been puzzling
scientists and there was much to be understood about the molecular mechanisms
governing its stability and function.
team at the University of Wisconsin, Madison led by cancer scientists Richard
A. Anderson and Vincent Cyrns reported the discovery of
. This enzyme is a nuclear phosphoinositide kinase
that when cell stress occurs either due to DNA damage or any other cause, the
enzyme gravitates towards p53 and produces PIP2 which also binds to it and
thereby, creates interaction
between p53 and molecules called small heat shock proteins.
heat shock proteins are good at stabilizing proteins and this type of strong
binding with p53 activates its cancer-causing role.
study also demonstrated that interrupting the PIP2 enzyme pathway can prevent
mutant p53 from accumulating and causing damage. Professor Anderson said that eliminating the mutated
form of p53 can prevent cancers.
says that despite p53 being one of the most frequently mutated genes causing
cancer, they still did not have any drug that targeted it.
team is now
on to discovering inhibitors for PIPK1-alpha which could be used to treat
tumors caused by p53 mutations. They hope to find methods to block the kinase
or other molecules that bind p53 and lead to accumulation of the protein in the
study was published in Nature Cell Biology
- UW team finds key to common cancer pathway in discovery that could unlock new therapies - (https://news.wisc.edu/uw-team-finds-key-to-common-cancer-pathway-in-discovery-that-could-unlock-new-therapies/)