Genome-wide CRISPR Screen to Identify Genes that Suppress Transformation in the Presence of Endogenous Kras^G12D.

ABSTRACT: Cooperating gene mutations are typically required to transform normal cells enabling growth in soft agar or in immunodeficient mice. For example, mutations in Kras and transformation-related protein 53 (Trp53) are known to transform a variety of mesenchymal and epithelial cells in vitro and in vivo. Identifying other genes that can cooperate with oncogenic Kras and substitute for Trp53 mutation has the potential to lead to new insights into mechanisms of carcinogenesis. Here, we applied a genome-wide CRISPR/Cas9 knockout screen in Kras^G12D immortalized mouse embryonic fibroblasts (MEFs) to search for genes that when mutated cooperate with oncogenic Kras to induce transformation. We also tested if mutation of the identified candidate genes could cooperate with Kras^G12D

SUBMITTER: Huang J 

PROVIDER: S-EPMC6868134 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature