Byoung-Ae Kim1, Hyeon-Gun Jee1, Jin Wook Yi1,2, Su-Jin Kim1,2, Young Jun Chai3, June Young Choi4, Kyu Eun Lee5,2. 1. Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea. 2. Department of Surgery, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Republic of Korea. 3. Department of Surgery, Seoul National University Boramae Medical Center, Seoul, Republic of Korea. 4. Department of Surgery, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Republic of Korea. 5. Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea kyueunlee@snu.ac.kr.
Abstract
BACKGROUND/AIM: The BRAFV600E mutation acts as an initiator of cancer development in papillary thyroid carcinoma (PTC). Gene expression changes caused by the BRAFV600E mutation may have an important role in thyroid cancer development. MATERIALS AND METHODS: To study genomic alterations caused by the BRAFV600E mutation, we made human thyroid cell lines that harbor the wild-type BRAF gene (Nthy/WT) and the V600E mutant-type BRAF gene (Nthy/V600E). RESULTS: Flow cytometry and western blotting showed stable transfection of the BRAF gene. In functional experiments, Nthy/V600E showed increased anchorage-independent growth and invasion through Matrigel, compared to Nthy/WT. Microarray analysis revealed that 2,441 genes were up-regulated in Nthy/V600E compared to Nthy/WT. Gene ontology analysis showed that the up-regulated genes were associated with cell adhesion, migration, and the ERK and MAPK cascade, and pathway analysis showed enrichment in cancer-related pathways. CONCLUSION: Our Nthy/WT and Nthy/V600E cell line pair could be a suitable model to study the molecular characteristics of BRAFV600E PTC. Copyright
BACKGROUND/AIM: The BRAFV600E mutation acts as an initiator of cancer development in papillary thyroid carcinoma (PTC). Gene expression changes caused by the BRAFV600E mutation may have an important role in thyroid cancer development. MATERIALS AND METHODS: To study genomic alterations caused by the BRAFV600E mutation, we made human thyroid cell lines that harbor the wild-type BRAF gene (Nthy/WT) and the V600E mutant-type BRAF gene (Nthy/V600E). RESULTS: Flow cytometry and western blotting showed stable transfection of the BRAF gene. In functional experiments, Nthy/V600E showed increased anchorage-independent growth and invasion through Matrigel, compared to Nthy/WT. Microarray analysis revealed that 2,441 genes were up-regulated in Nthy/V600E compared to Nthy/WT. Gene ontology analysis showed that the up-regulated genes were associated with cell adhesion, migration, and the ERK and MAPK cascade, and pathway analysis showed enrichment in cancer-related pathways. CONCLUSION: Our Nthy/WT and Nthy/V600E cell line pair could be a suitable model to study the molecular characteristics of BRAFV600E PTC. Copyright
Authors: Cleo Mesa; Mana Mirza; Norisato Mitsutake; Maureen Sartor; Mario Medvedovic; Craig Tomlinson; Jeffrey A Knauf; Georg F Weber; James A Fagin Journal: Cancer Res Date: 2006-07-01 Impact factor: 12.701
Authors: Hongxia Sun; Wen-Cheng Chung; Seung-Hee Ryu; Zhenlin Ju; Hai T Tran; Edward Kim; Jonathan M Kurie; Ja Seok Koo Journal: Cancer Prev Res (Phila) Date: 2008-10