cross-regulation between oncogenic brafv600e kinase and the mst1 pathway in papillary thyroid carcinomacross-regulation致癌brafv600e激酶和mst1通路之间在乳头状甲状腺癌.pdf

Cross-Regulation between Oncogenic BRAFV600E Kinase and the MST1 Pathway in Papillary Thyroid Carcinoma 1,3. 1. 1. 1 2 1 Seong Jin Lee , Min Hee Lee , Dong Wook Kim , SeongEun Lee , Songmei Huang , Min Jeong Ryu , 1 1 1 1,4 5 Yong Kyung Kim , Sung Jin Kim , Soung Jung Kim , Jung Hwan Hwang , Sangphil Oh , Heeyeong 3 2 5 6 1 Cho , Jin Man Kim , Dae-Sik Lim , Young Suk Jo *, Minho Shong * 1 Department of Internal Medicine, Chungnam National University School of Medicine, Daejeon, Republic of Korea, 2 Department of Pathology, Chungnam National University School of Medicine, Daejeon, Republic of Korea, 3 Pharmacology Research Center, Korea Research Institute of Chemical Technology, Daejeon, Republic of Korea, 4 Animal Model Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea, 5 Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea, 6 Research Center for Endocrine and Metabolic Diseases, Chungnam National University Hospital, Daejeon, Republic of Korea Abstract Background: The BRAFV600E mutation leading to constitutive signaling of MEK-ERK pathways causes papillary thyroid cancer (PTC). Ras association domain family 1A (RASSF1A), which is an important regulator of MST1 tumor suppressor pathways, is inactivated by hypermethylation