Abstract:
:The aminoacyl tRNA synthetase complex-interacting multifunctional protein 2 (AIMP2) splice variant designated DX2 is induced by cigarette smoke carcinogens and is often detected in human lung cancer specimens. However, the function of DX2 in lung carcinogenesis is obscure. In this study, we found that DX2 expression was induced by oncogenes in human lung cancer tissues and cells. DX2 prevented oncogene-induced apoptosis and senescence and promoted drug resistance by directly binding to and inhibiting p14/ARF. Through chemical screening, we identified SLCB050, a novel compound that blocks the interaction between DX2 and p14/ARF in vitro and in vivo SLCB050 reduced the viability of human lung cancer cells, especially small cell lung cancer cells, in a p14/ARF-dependent manner. Moreover, in a mouse model of K-Ras-driven lung tumorigenesis, ectopic expression of DX2 induced small cell and non-small cell lung cancers, both of which could be suppressed by SLCB050 treatment. Taken together, our findings show how DX2 promotes lung cancer progression and how its activity may be thwarted as a strategy to treat patients with lung cancers exhibiting elevated DX2 levels. Cancer Res; 76(16); 4791-804. ©2016 AACR.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Oh AY,Jung YS,Kim J,Lee JH,Cho JH,Chun HY,Park S,Park H,Lim S,Ha NC,Park JS,Park CS,Song GY,Park BJdoi
10.1158/0008-5472.CAN-15-1025subject
Has Abstractpub_date
2016-08-15 00:00:00pages
4791-804issue
16eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-15-1025journal_volume
76pub_type
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