LKB1 drives stasis and C/EBP-mediated reprogramming to an alveolar type II fate in lung cancer

LKB1 drives stasis and C/EBP-mediated reprogramming to an alveolar type II fate in lung cancer

LKB1 is among the most frequently altered tumor suppressors in lung adenocarcinoma. Inactivation of Lkb1 accelerates the growth and progression of oncogenic KRAS-driven lung tumors in mouse models. However, the molecular mechanisms by which LKB1 constrains lung tumorigenesis and whether the cancer state that stems from Lkb1 deficiency can be reverted remains unknown. To identify the processes governed by LKB1 in vivo, we generated an allele which enables Lkb1 inactivation at tumor initiation and subsequent Lkb1 restoration in established tumors. Restoration of Lkb1 in oncogenic KRAS-driven lung tumors suppressed proliferation and led to tumor stasis.

View the full article and citation at: https://pubmed.ncbi.nlm.nih.gov/37696956/