Research lead
Scientists at the Karolinska Institutet have shown that a previously unknown gene, Wrap53, controls the activity of p53, the gene that ensures cells with damaged DNA either repair themselves or undergo programmed cell death. When p53 itself is damaged, as is the case in roughly half of all tumours, cells on their way to becoming cancerous survive.
The researchers have demonstrated that Wrap53 gives rise to antisense RNA, which is necessary for the production of sufficient quantities of p53 protein in the event of DNA damage.
Marianne Farnebo, one of the scientists involved in the study, says that damage to Wrap53 can indirectly cause cancer, making it a new potential target for cancer drugs. “Mutations in the p53 gene contribute to about half of all cancer cases. In the remaining half, p53 is probably inactivated in other ways, such as damage to Wrap53 knocking out the production of the p53 protein.”