title: ID1 Controls Aggressiveness of Salivary Gland Cancer Cells via Crosstalk of IGF and AKT Pathways.
abstract: BACKGROUND
  Inhibitor of differentiation or DNA binding 1 (ID1) is overexpressed in human salivary gland cancer (SGC). The insulin growth factor (IGF) system is an attractive target in cancer control because it is associated with various cancer progressions.
  
  
  METHODS
  The human SGC cell line HSY with abundant ID1 was used. ID1 knockdown and its effect on the IGF system were investigated. Cell proliferation and invasion, as well as associated protein expression, were analyzed. Phospho-AKT was also evaluated.
  
  
  RESULTS
  ID1 knockdown reduced cell proliferation and invasion, while the expression of proteins associated with malignant phenotypes was altered. IGF-II expression was suppressed, suggesting that this system is one of the mechanisms underlying effects of ID1 in SGC cells. c-Myc was up-regulated, whereas p21 and p27 were down-regulated. Moreover, phospho-AKT was reduced in ID1-knockeddown cells.
  
  
  CONCLUSIONS
  ID1 down-regulation induced parallel changes in the IGF and AKT pathways. The crosstalk of these pathways may enhance malignant phenotypes in SGCs.
authors.affiliation: Section of Oral & Maxillofacial Surgery, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, Japan tomoki@dent.kyushu-u.ac.jp.
authors.forename: Tomoki
authors.initials: T
authors.lastname: Sumida
authors.affiliation: Section of Oral & Maxillofacial Surgery, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
authors.forename: Y U
authors.initials: YU
authors.lastname: Kamata
authors.affiliation: Section of Oral & Maxillofacial Surgery, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Kobayashi
authors.affiliation: Department of Oral & Maxillofacial Surgery, Ehime University Graduate School of Medicine, Ehime, Japan.
authors.forename: Akiko
authors.initials: A
authors.lastname: Ishikawa
authors.affiliation: Section of Oral & Maxillofacial Surgery, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
authors.forename: Yoshihide
authors.initials: Y
authors.lastname: Mori
mesh_terms: D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D006801:Humans; D051798:Inhibitor of Differentiation Protein 1 / Q000235:genetics*; D007328:Insulin / Q000235:genetics* / Q000378:metabolism; D007335:Insulin-Like Growth Factor II / Q000096:biosynthesis / Q000235:genetics*; D009361:Neoplasm Invasiveness / Q000235:genetics; D051057:Proto-Oncogene Proteins c-akt / Q000096:biosynthesis* / Q000235:genetics; D016271:Proto-Oncogene Proteins c-myc / Q000096:biosynthesis; D012468:Salivary Gland Neoplasms / Q000235:genetics* / Q000473:pathology; D015398:Signal Transduction
chemical_list: C497453:ID1 protein, human; D051798:Inhibitor of Differentiation Protein 1; D007328:Insulin; C489427:MYC protein, human; D016271:Proto-Oncogene Proteins c-myc; D007335:Insulin-Like Growth Factor II; D051057:Proto-Oncogene Proteins c-akt
keywords: AKT; inhibitor of differentiation; insulin-like growth factor; invasion; proliferation; salivary gland cancer