Mutant IDH1 is required for IDH1 mutated tumor cell growth

• DOI: 10.18632/oncotarget.577
• Publication Date: 2015-09-16T21:49:21Z
• Authors: Genglin Jin; Christopher J. Pi...; Lee H. Chen; Giselle Y. Lopez; Christopher G. Du...; Jie Feng; Ivan Spasojevic; Darell D. Bigner; Yiping He; Hai Yan
• Keywords: Isocitrate dehydrogenase; IDH2; Clonogenic assay

// Genglin Jin 1 , Christopher J. Pirozzi Lee H. Chen Giselle Y. Lopez G. Duncan Jie Feng Ivan Spasojevic 2 Darell D. Bigner Yiping He and Hai Yan The Preston Robert Tisch Brain Tumor Center, Pediatric Foundation Institute, Department of Pathology, Clinical Pharmacology Laboratory, Duke Cancer Institute Medicine/Oncology University Medical Durham, North Carolina, USA Correspondence: Yan, email: Keywords : IDH1, cell survival Received July 27, 2012, Accepted August 04, Published 09, 2012 Abstract Frequent somatic hotspot mutations in isocitrate dehydrogenase (IDH1) have been identified gliomas, acute myeloid leukemias, chondrosarcomas, other cancers, providing a likely avenue for targeted cancer therapy. However, whether mutant IDH1 protein is required maintaining mutated tumor growth remains unknown. Here, using genetically engineered inducible system, we report that selective suppression endogenous expression HT1080, fibrosarcoma line with native R132C heterozygous mutation, significantly inhibits proliferation decreases clonogenic potential. Our findings offer insights into changes may contribute to the inhibition strong preclinical rationale utilizing as valid therapeutic target.