title: Differentially regulated genes in MEN1-transfected BON cells using RT-differential display and oligonucleotide microarrays.
abstract: BACKGROUND
  Apart from inactivation of the MEN1 gene, the molecular mechanisms involved in tumorigenesis of the endocrine organs and MEN1-associated non-endocrine lesions remain unknown.
  
  
  METHODS
  In order to learn more about down-stream effects upon MEN1 gene inactivation BON1 cells were transfected with a MEN1 gene construct (BON/M1C), and both RT-differential display and oligonucleotide microarrays were performed.
  
  
  RESULTS
  Three genes (SMARCC1, OVCA2 and SRp55) found to be differentially regulated on differential display were corroborated by northern blots on cell line RNA when comparing MEN1 transfected cells with control (empty vector transfection). When comparing two different passages of BON/M1C with two passages of vector control using oligonucleotide microarrays, 25 up-regulated genes and 64 down-regulated genes could be found using a cut-off of >or=1.6 times.
  
  
  CONCLUSIONS
  These findings might contribute to the understanding of the molecular pathways involved in MEN1 tumorigenesis, and may also provide knowledge of genes involved in sporadic endocrine tumorigenesis.
authors.affiliation: Department of Medical Sciences, University Hospital, 751 85 Uppsala, Sweden.
authors.forename: Juan R
authors.initials: JR
authors.lastname: Lopez-Egido
authors.forename: Yi
authors.initials: Y
authors.lastname: Wang
authors.forename: Malin
authors.initials: M
authors.lastname: Grönberg
authors.forename: Per
authors.initials: P
authors.lastname: Grimfjärd
authors.forename: Shu
authors.initials: S
authors.lastname: Wang
authors.forename: Peter
authors.initials: P
authors.lastname: Stålberg
authors.forename: Britt
authors.initials: B
authors.lastname: Skogseid
mesh_terms: D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism*; D015152:Blotting, Northern; D045744:Cell Line, Tumor; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D015778:Minor Histocompatibility Antigens; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D010190:Pancreatic Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D010750:Phosphoproteins / Q000235:genetics / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016601:RNA-Binding Proteins; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000068103:Serine-Arginine Splicing Factors; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014162:Transfection; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D014408:Biomarkers, Tumor; C121987:DPH1 protein, human; C105373:MEN1 protein, human; D015778:Minor Histocompatibility Antigens; D009687:Nuclear Proteins; D010750:Phosphoproteins; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D016601:RNA-Binding Proteins; C101681:SMARCC1 protein, human; C489470:SRSF6 protein, human; D014157:Transcription Factors; D025521:Tumor Suppressor Proteins; D000068103:Serine-Arginine Splicing Factors