title: Multiple proliferation-survival signalling pathways are simultaneously active in BRAF V600E mutated thyroid carcinomas.
abstract: OBJECTIVE
  BRAF is an oncogene which involves in pathogenesis of many thyroid carcinomas.The aim of our study was to investigate whether the downstream signalling pathway of BRAF and AKT kinase signalling pathways were active in BRAF V600E mutated thyroid carcinoma cells.
  
  
  METHODS
  Five thyroid (papillary and undifferentiated) carcinoma cell lines and one non-cancer thyroid cell line were screened for their BRAF V600E mutation status by immunofluorescent staining and Western blot. BRAF V600E mutated thyroid carcinoma cell lines were used to test the activation status of both ERK and AKT kinase proteins through immunofluorescent studies and Western blots.
  
  
  RESULTS
  Expressions of BRAF V600E mutated protein were confirmed in four thyroid (papillary and undifferentiated) carcinoma cell lines. In these cell lines, both active ERK and active AKT kinase proteins were found in BRAF V600E mutated thyroid carcinoma cells by immunofluorescent staining and Western blots experiments.
  
  
  CONCLUSIONS
  In BRAF V600E mutated thyroid carcinomas, active ERK and active AKT kinase proteins were noted. They are able to stimulate multiple downstream signalling pathways which ultimately result in increased proliferation and survival activities for cancer cells. Therefore, consideration needs to put on multiple targets when deciding molecular target therapies for patients with BRAF V600E mutated thyroid carcinoma.
authors.affiliation: Cancer Molecular Pathology, School of Medicine, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
authors.forename: Md Atiqur
authors.initials: MA
authors.lastname: Rahman
authors.affiliation: Cancer Molecular Pathology, School of Medicine, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
authors.forename: Ali
authors.initials: A
authors.lastname: Salajegheh
authors.affiliation: Cancer Molecular Pathology, School of Medicine, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia; Genomics Research Centre, Institute of Health and Biomedical Innovation, Faculty of Health, Queensland University of Technology, Brisbane, Queensland, Australia.
authors.forename: Robert Anthony
authors.initials: RA
authors.lastname: Smith
authors.affiliation: Cancer Molecular Pathology, School of Medicine, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia; Pathology Queensland and Gold Coast University Hospital, Gold Coast, Queensland, Australia. Electronic address: a.lam@griffith.edu.au.
authors.forename: Alfred King-yin
authors.initials: AK
authors.lastname: Lam
mesh_terms: D002291:Carcinoma, Papillary / Q000235:genetics / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D006801:Humans; D020935:MAP Kinase Signaling System / Q000235:genetics; D009154:Mutation / Q000235:genetics*; D051058:Oncogene Protein v-akt / Q000378:metabolism; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics*; D013964:Thyroid Neoplasms / Q000235:genetics* / Q000473:pathology
chemical_list: C482119:BRAF protein, human; D051058:Oncogene Protein v-akt; D048493:Proto-Oncogene Proteins B-raf
keywords: AKT; BRAF; ERK; Thyroid carcinoma; cell signalling pathway