title: The SGBS cell strain as a model for the in vitro study of obesity and cancer.
abstract: BACKGROUND
  The murine adipocyte cell line 3T3-L1 is well characterised and used widely, while the human pre-adipocyte cell strain, Simpson-Golabi-Behmel Syndrome (SGBS), requires validation for use in human studies. Obesity is currently estimated to account for up to 41 % of the worldwide cancer burden. A human in vitro model system is required to elucidate the molecular mechanisms for this poorly understood association. This work investigates the relevance of the SGBS cell strain for obesity and cancer research in humans.
  
  
  METHODS
  Pre-adipocyte 3T3-L1 and SGBS were differentiated according to standard protocols. Morphology was assessed by Oil Red O staining. Adipocyte-specific gene expression was measured by qPCR and biochemical function was assessed by glycerol-3-phosphate dehydrogenase (GPDH) enzyme activity. Differential gene expression in oesophageal adenocarcinoma cell line OE33 following co-culture with SGBS or primary omental human adipocytes was investigated using Human Cancer Profiler qPCR arrays.
  
  
  RESULTS
  During the process of differentiation, SGBS expressed higher levels of adipocyte-specific transcripts and fully differentiated SGBS expressed more similar morphology, transcript levels and biochemical function to primary omental adipocytes, relative to 3T3-L1. Co-culture with SGBS or primary omental adipocytes induced differential expression of genes involved in adhesion (ITGB3), angiogenesis (IGF1, TEK, TNF, VEGFA), apoptosis (GZMA, TERT) and invasion and metastasis (MMP9, TIMP3) in OE33 tumour cells.
  
  
  CONCLUSIONS
  Comparable adipocyte-specific gene expression, biochemical function and a shared induced gene signature in co-cultured OE33 cells indicate that SGBS is a relevant in vitro model for obesity and cancer research in humans.
authors.affiliation: Department of Surgery, Trinity Centre for Health Sciences, Institute of Molecular Medicine, St James' Hospital, Trinity College Dublin, Ireland.
authors.forename: Emma H
authors.initials: EH
authors.lastname: Allott
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Oliver
authors.forename: Joanne
authors.initials: J
authors.lastname: Lysaght
authors.forename: Steven G
authors.initials: SG
authors.lastname: Gray
authors.forename: John V
authors.initials: JV
authors.lastname: Reynolds
authors.forename: Helen M
authors.initials: HM
authors.lastname: Roche
authors.forename: Graham P
authors.initials: GP
authors.lastname: Pidgeon
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology* / Q000378:metabolism / Q000502:physiology*; D050156:Adipogenesis / Q000235:genetics / Q000502:physiology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000473:pathology*; D002460:Cell Line; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D040181:Genetic Diseases, X-Linked / Q000473:pathology*; D005877:Gigantism / Q000473:pathology*; D006330:Heart Defects, Congenital / Q000473:pathology*; D006801:Humans; D008607:Intellectual Disability / Q000473:pathology*; D051379:Mice; D046228:Microarray Analysis; D008962:Models, Theoretical; D009369:Neoplasms / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D009765:Obesity / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D061251:Primary Cell Culture