Regulation of HIF1α expression by a natural compound; a new hnRNP involvement Bo Yeon Kim1 ,Yukihiro Asami1 , Nak Kyun Soung1 , Hae Min Kim1 , Jae Hyuk Jang1 , N.R. Themmegowda1 , Jong Seog Ahn1 and Kyung Lee2 1 Korea Research Institute of Bioscience & Biotechnology, Korea 2 Department of Pharmacology, DongKook University, Korea Hypoxia induces HIF1aexpression, leading to the malignant cell transformation. In screening of inhibitors against HIF1aexpression using a reporter gene assay system, a moracin derivative, MOA, was found to strongly reduce the level of HIF1ain HeLa cellsboth in hypoxia-mimetic CoCl2 treatment and under hypoxic conditions. Identification of binding proteins using agarose-bead conjugated MOA(AC-685) combined with subsequent MS data revealed several proteins affected by MOA. AC-685 co-localized with a nuclear hnRNPX protein in CoCl2 treated HeLa cells. Amongst several cytoplasmic or nuclear proteins, hnRNPX was only found to be responsible for CoCl2 -induced HIF1α expression as supported by siRNA depletion of the protein. Cancer growth was also found to be reduced in a genograft animal model. This study suggests that regulation of HIF1aexpression by MOAunder the control of hnRNP would be a novel approach to cancer treatment in hypoxic environment. Biography: Dr. Bo Yeon Kim got Ph.D degree at Seoul National University in 1996. After the research fellow experience at Georgetown University, 2000-2003, he continued his work at Korea Research Institute of Bioscience & Biotechnology (KRIBB) for about 26 yrs so far. Major research focuses on identification of new cancer signaling pathways and development of a new anticancer drug with low side effect. In recent 5 years, He has made more than 65 publications, including Nature Cell Biology (2015), Autophagy (2016, 2013), Proc Natl Acad Sci, USA (2013), J Am Chem Soc (2011), J Biol Chem (2013, 2012), and under revision papers (Nature Communicaitons, EMBO Reports, Autophagy) as a corresponding author.