OGFOD1 is required for breast cancer cell proliferation and is associated with poor prognosis in breast cancer

// Jae-Hwan Kim 1,* , Soon-Min Lee 1,* , Jong-Hyuk Lee 1,* , Sohyun Chun 4,* , Byung-Hee Kang 1,* , Sojung Kwak 1,* , Jae-Seok Roe 1 , Tae Wan Kim 1 , Hyunsoo Kim 1 , Woo Ho Kim 2 , Eun-Jung Cho 3 and Hong-Duk Youn 1,4 1 National Creative Research Center for Epigenome Reprogramming Network, Department of Biomedical Sciences, Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, Republic of Korea 2 Department of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea 3 College of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea 4 Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science, Seoul National University, Seoul, Republic of Korea * These authors have contributed equally to this work Correspondence to: Hong-Duk Youn, email: // Keywords : OGFOD1, G2/M phase, cell cycle, breast cancer Received : Decmber 05, 2014 Accepted : March 11, 2015 Published : March 29, 2015 Abstract 2-oxogluatrate and Fe(II)-dependent oxygenase domain-containing protein 1 (OGFOD1) was recently revealed to be a proline hydroxylase of RPS23 for translational termination. However, OGFOD1 is nuclear, whereas translational termination occurs in the cytoplasm, raising the possibility of another function of OGFOD1 in the nucleus. In this study, we demonstrate that OGFOD1 is involved in cell cycle regulation. OGFOD1 knockdown in MDA-MB-231 breast cancer cells significantly impeded cell proliferation and resulted in the accumulation of G1 and G2/M cells by decreasing the mRNA levels of G1/S transition- and G2/M-related transcription factors and their target genes. We also confirmed that OGFOD1 is highly expressed in breast cancer tissues by bioinformatic analysis and immunohistochemistry. Thus, we propose that OGFOD1 is required for breast cancer cell proliferation and is associated with poor prognosis in breast cancer.