title: Overexpression of wild-type THRbeta1 suppresses the growth and invasiveness of human papillary thyroid cancer cells.
abstract: BACKGROUND
  Thyroid hormone receptors (THRs) are transcription factors which regulate cell growth and differentiation. The compromised function of THRs has been reported in several human malignancies, suggesting their implication in carcinogenesis.
  
  
  METHODS
  Using an adenoviral delivery system, THRbeta1 was expressed in human papillary thyroid cancer cell lines and corresponding biological and molecular changes were analyzed.
  
  
  RESULTS
  THRPbeta1-dependent transactivation activity is diminished in thyroid cancer cell lines. Its restoration suppresses the proliferation, causes G1 arrest, depresses DNA synthesis and decreases invasiveness of cancer cells paralleled by the attenuation of AKT and MAPK signaling, and reduction of cyclin D1 levels.
  
  
  CONCLUSIONS
  The alteration of THRbeta1 functioning is an important change in human well-differentiated thyroid carcinomas, affecting tumor cell growth and contributing to the malignant potential of cancer cells.
authors.affiliation: Departments of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
authors.forename: Ilya
authors.initials: I
authors.lastname: Sedliarou
authors.forename: Michiko
authors.initials: M
authors.lastname: Matsuse
authors.forename: Vladimir
authors.initials: V
authors.lastname: Saenko
authors.forename: Tatiana
authors.initials: T
authors.lastname: Rogounovitch
authors.forename: Yuka
authors.initials: Y
authors.lastname: Nakazawa
authors.forename: Norisato
authors.initials: N
authors.lastname: Mitsutake
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Namba
authors.forename: Yuji
authors.initials: Y
authors.lastname: Nagayama
authors.forename: Shunichi
authors.initials: S
authors.lastname: Yamashita
mesh_terms: D000256:Adenoviridae / Q000235:genetics; D002291:Carcinoma, Papillary / Q000201:enzymology / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D002453:Cell Cycle / Q000502:physiology; D048708:Cell Growth Processes / Q000502:physiology; D045744:Cell Line, Tumor; D006801:Humans; D020935:MAP Kinase Signaling System; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D009361:Neoplasm Invasiveness; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D037042:Thyroid Hormone Receptors beta / Q000096:biosynthesis* / Q000235:genetics; D013964:Thyroid Neoplasms / Q000201:enzymology / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D015533:Transcriptional Activation; D014162:Transfection
chemical_list: D037042:Thyroid Hormone Receptors beta; D051057:Proto-Oncogene Proteins c-akt; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020780:Matrix Metalloproteinase 9; D020781:Matrix Metalloproteinase 1