| First Author | Eichner LJ | Year | 2019 |
| Journal | Cell Metab | Volume | 29 |
| Issue | 2 | Pages | 285-302.e7 |
| PubMed ID | 30415923 | Mgi Jnum | J:272057 |
| Mgi Id | MGI:6282687 | Doi | 10.1016/j.cmet.2018.10.005 |
| Citation | Eichner LJ, et al. (2019) Genetic Analysis Reveals AMPK Is Required to Support Tumor Growth in Murine Kras-Dependent Lung Cancer Models. Cell Metab 29(2):285-302.e7 |
| abstractText | AMPK, a conserved sensor of low cellular energy, can either repress or promote tumor growth depending on the context. However, no studies have examined AMPK function in autochthonous genetic mouse models of epithelial cancer. Here, we examine the role of AMPK in murine Kras(G12D)-mediated non-small-cell lung cancer (NSCLC), a cancer type in humans that harbors frequent inactivating mutations in the LKB1 tumor suppressor-the predominant upstream activating kinase of AMPK and 12 related kinases. Unlike LKB1 deletion, AMPK deletion in Kras(G12D) lung tumors did not accelerate lung tumor growth. Moreover, deletion of AMPK in Kras(G12D) p53(f/f) tumors reduced lung tumor burden. We identified a critical role for AMPK in regulating lysosomal gene expression through the Tfe3 transcription factor, which was required to support NSCLC growth. Thus, AMPK supports the growth of Kras(G12D)-dependent lung cancer through the induction of lysosomes, highlighting an unrecognized liability of NSCLC. |
