Oncotarget

Brief Reports:

Mutant IDH1 is required for IDH1 mutated tumor cell growth

Genglin Jin, Christopher J. Pirozzi, Lee H. Chen, Christopher G. Duncan, Giselle Y. Lopez, Jie Feng, Ivan Spasojevic, Darell D. Bigner, Yiping He and Hai Yan _

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Oncotarget. 2012; 3:774-782. https://doi.org/10.18632/oncotarget.577

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Abstract

Genglin Jin1, Christopher J. Pirozzi1, Lee H. Chen1, Giselle Y. Lopez1, Christopher G. Duncan1, Jie Feng1, Ivan Spasojevic2, Darell D. Bigner1, Yiping He1, and Hai Yan1

1 The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation Institute, and The Department of Pathology,

2 The Clinical Pharmacology Laboratory, Duke Cancer Institute and Department of Medicine/Oncology, Duke University Medical Center, Durham, North Carolina, USA

Correspondence:

Hai Yan, email:

Keywords: IDH1, cell survival

Received: July 27, 2012, Accepted: August 04, 2012, Published: August 09, 2012

Abstract

Frequent somatic hotspot mutations in isocitrate dehydrogenase 1 (IDH1) have been identified in gliomas, acute myeloid leukemias, chondrosarcomas, and other cancers, providing a likely avenue for targeted cancer therapy. However, whether mutant IDH1 protein is required for maintaining IDH1 mutated tumor cell growth remains unknown. Here, using a genetically engineered inducible system, we report that selective suppression of endogenous mutant IDH1 expression in HT1080, a fibrosarcoma cell line with a native IDH1R132C heterozygous mutation, significantly inhibits cell proliferation and decreases clonogenic potential. Our findings offer insights into changes that may contribute to the inhibition of cell proliferation and offer a strong preclinical rationale for utilizing mutant IDH1 as a valid therapeutic target.


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