Aptamer-targeted CRISPR **MDM2 knockout** induces cell cycle arrest and TAp73 in patient cancer cells, p53-independent.
A targeting delivery platform for the mapping of responses to p53-independent intervention in heterogeneous patient cancer cells.
Abstract
An aptamer-targeted CRISPR platform for MDM2 knockout effectively induces cell cycle arrest and upregulates anti-tumor TAp73 in patient-derived cancer cells, irrespective of their p53 status.
