SYNCRIP promotes cell cycle progression and lung tumorigenesis by modulating AURKB translation  

作　　者：Hyeon Ji Kim Hye Guk Ryu Mingyu Kang Namgyu Lee Hyo-Jin Kim Dahye Lee Chaeuk Chung Sangjune Kim Kyung-Ha Lee Wanil Kim Jin-Seok Byun Kyong-Tai Kim Do-Yeon Kim 

机构地区：[1]Department of Pharmacology,School of Dentistry,Kyungpook National University,Daegu,Republic of Korea [2]Department of Life Sciences,Pohang University of Science and Technology(POSTECH),Pohang,Republic of Korea [3]Division of Cancer Biology,Research Institute,National Cancer Center,Goyang,Republic of Korea [4]Department of Biomedical Science&Systems Biology,Dankook University,Cheonan,Republic of Korea [5]ProGen.Co.,Ltd.,Seoul,Republic of Korea [6]Division of Pulmonology and Critical Care Medicine,Department of Internal Medicine,College of Medicine,Chungnam National University,Daejeon,Republic of Korea [7]Department of Biological Sciences and Biotechnology,Chungbuk National University,Cheongju,Republic of Korea [8]Department of Molecular Biology,Pusan National University,Busan,Republic of Korea [9]Department of Biochemistry,Department of Convergence Medical Science,Institute of Medical Science,School of Medicine,Gyeongsang National University,Jinju,Republic of Korea [10]Department of Oral Medicine,School of Dentistry,Kyungpook National University,Daegu,Republic of Korea [11]Generative Genomics Research Center,Global Green Research&Development Center,Handong Global University,Pohang,Republic of Korea

出　　处：《Cancer Communications》2025年第2期138-142,共5页癌症通讯(英文)

基　　金：supported by the National Research Foundation of Korea(NRF)grant funded by the Korea government(MSIT)(2022R1C1C1006181,2022R1A6A3A13071217,and RS-2023-00272063).

摘　　要：Dysregulation of cellular processes,such as cell division and proliferation,is a hallmark of cancer and is driven by the aberrant expression of cell cyclerelated genes[1].Aurora kinase B(AURKB),due to its pivotal role in mitotic progression,has been implicated in various cancers.Overexpression or hyperactivation of AURKB significantly contributes to tumorigenesis and cancer progression[2].Although mechanisms that enhance AURKB activity,including binding to INCENP,autophosphorylation[3],and ubiquitination by TRAF6[4],have been extensively investigated,regulation of AURKB synthesis,particularly mRNA translation,remains unclear.The translation of eukaryotic mRNAs typically occurs either through cap-dependent scanning or through direct ribosomal binding to specialized RNA elements known as internal ribosome entry sites(IRES).IRES-mediated translation is strongly influenced by specific RNA-binding proteins,known as IRES trans-acting factors(ITAFs).SYNCRIP(Synaptotagmin-binding cytoplasmic RNA-interacting protein),also known as hnRNP Q,has been identified as an ITAF[5],integrating various aspects of RNA metabolism with key cellular processes.Here,we aim to elucidate the mechanism of AURKB mRNA translation and investigate whether SYNCRIP regulates AURKB mRNA translation in lung cancer.

关 键 词：TRANSLATION HAS SUCH 

分 类 号：H31[语言文字—英语]