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http://dx.doi.org/10.14348/molcells.2019.0099

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

Park, Choa (Department of Biological Sciences, Sookmyung Women's University)
Lee, Yejin (Department of Biological Sciences, Sookmyung Women's University)
Je, Soyeon (Department of Biological Sciences, Sookmyung Women's University)
Chang, Shengzhi (Department of Biological Sciences, Sookmyung Women's University)
Kim, Nayoung (Department of Biological Sciences, Sookmyung Women's University)
Jeong, Euna (Research Institute of Women's Health, Sookmyung Women's University)
Yoon, Sukjoon (Department of Biological Sciences, Sookmyung Women's University)
Publication Information
Molecules and Cells / v.42, no.11, 2019 , pp. 804-809 More about this Journal
Abstract
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-of-function 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.
Keywords
Enolase 3; lung adenocarcinoma; STK11 loss-of-function mutation;
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