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Mol Cells. 2019 Nov 7. doi: 10.14348/molcells.2019.0099. [Epub ahead of print]

Overexpression and Selective Anticancer Efficacy of ENO3 in STK11 Mutant Lung Cancers.

Park C1,2, Lee Y1,2, Je S1,2, Chang S1, Kim N1, Jeong E3, Yoon S1,3.

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Department of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
These authors contributed equally to this work.
Research Institute of Women's Health, Sookmyung Women's University, Seoul 04310, Korea.


Oncogenic gain-of-function mutations are clinical biomarkers for most targeted therapies, as well as represent direct targets for drug treatment. Although loss-of-function mutations involving the tumor suppressor gene, STK11 (LKB1) are important in lung cancer progression, STK11 is not the direct target for anticancer agents. We attempted to identify cancer transcriptome signatures associated with STK11 loss-offunction mutations. Several new sensitive and specific gene expression markers (ENO3, TTC39C, LGALS3, and MAML2) were identified using two orthogonal measures, i.e., fold change and odds ratio analyses of transcriptome data from cell lines and tissue samples. Among the markers identified, the ENO3 gene over-expression was found to be the direct consequence of STK11 loss-of-function. Furthermore, the knockdown of ENO3 expression exhibited selective anticancer effect in STK11 mutant cells compared with STK11 wild type (or recovered) cells. These findings suggest that ENO3 -based targeted therapy might be promising for patients with lung cancer harboring STK11 mutations.


Enolase 3; STK11 loss-offunction mutation; lung adenocarcinoma

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