The BCL-2 family member BOK promotes KRAS-driven lung cancer progression in a p53-dependent manner.

ABSTRACT: A variety of cancer entities are driven by KRAS mutations, which remain difficult to target clinically. Survival pathways, such as resistance to cell death, may represent a promising treatment approach in KRAS mutated cancers. Based on the frequently observed genomic deletions of BCL-2-related ovarian killer (BOK) in cancer patients, we explored the function of BOK in a mutant Kras^G12D-driven murine model of lung cancer. Using Kras^G12D/+ Bok^-/- mice, we observed an overall tumor-promoting function of BOK in vivo. Specifically, loss of BOK reduced proliferation both in cell lines in vitro as well as in Kras^G12D-driven tumor lesions in vivo. During tumor development in vivo, loss of BOK resulted in a lower tumor burden, with fewer, smaller, and les

SUBMITTER: Meinhardt AL 

PROVIDER: S-EPMC8881215 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature