Loss of PIK3CA allows <i>in vitro</i> growth but not <i>in vivo</i> progression of KRAS mutant lung adenocarcinoma in a syngeneic orthotopic implantation model.

ABSTRACT: Constitutively active KRAS mutations are highly prevalent in lung cancers, but the direct role of its downstream phosphatidylinositol 3-kinase (PI3K) pathway in tumor progression remains unclear. A previous study established the requirement for PIK3CA, the alpha catalytic isoform, in lung tumor development in mouse models with an intact Trp53 tumor suppressor. In this study, we further investigated the requirement for PIK3CA for tumor growth both in vitro and in vivo . We first generated a "KPA" cell line by genetically deleting Pik3ca from a murine lung adenocarcinoma "KP" cell line harboring oncogenic Kras ^G12D and lacking Trp53 . We found that Pik3ca is not required for cell survival and growth in vitro , even und

SUBMITTER: Booth AL 

PROVIDER: S-EPMC12889443 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature