title: Overexpressed in anaplastic thyroid carcinoma-1 (OEATC-1) as a novel gene responsible for anaplastic thyroid carcinoma.
abstract: BACKGROUND
  Anaplastic thyroid carcinoma (ATC) is one of the most fulminant human malignancies. However, the molecular carcinogenic mechanisms of ATC are understood poorly. Recently, the authors performed a cyclic DNA (cDNA) microarray analysis with 11 anaplastic thyroid carcinoma cell lines (ACLs) and discovered several novel responsible genes for ACLs and ATC. From the extended list, they focused on hypothetical and anonymous genes and investigated a novel gene, named the overexpressed in anaplastic thyroid carcinoma-1 (OEATC-1) gene.
  
  
  METHODS
  To investigate the role of the OEATC-1 gene in ATC carcinogenesis, first, the expression levels of OEATC-1 in ACLs, in various types of carcinoma cell lines, and in normal human tissues were examined with reverse transcriptase-polymerase chain reaction analysis. To explore the effect of OEATC-1 in ATC development, a cell-growth assay was performed with KTA2 cells under OEATC-1 gene silencing using small-interfering RNA (siRNA).
  
  
  RESULTS
  OEATC-1 was overexpressed significantly in ACLs and in other types of carcinoma cell lines with various expression levels. Conversely, in normal human tissues, OEATC-1 was expressed weakly in placenta, kidney, spleen, thymus, small intestine, and thyroid gland. To evaluate the effects of OEATC-1 on tumor cell growth, gene silencing was caused by transfecting the plasmid-generating siRNA effect to KTA2 cells. Consequently, the silencing of OEATC-1 significantly suppressed the cell growth compared with controls.
  
  
  CONCLUSIONS
  The current results indicated that OEATC-1 may have some oncogenic or cell growth-promoting function in ACL. OEATC-1 is considered a novel responsible gene in ATC.
authors.affiliation: Department of Molecular Biology, Institute of Gerontology, Nippon Medical School, Kanagawa, Japan.
authors.forename: Kazunori
authors.initials: K
authors.lastname: Mizutani
authors.forename: Masamitsu
authors.initials: M
authors.lastname: Onda
authors.forename: Shinichi
authors.initials: S
authors.lastname: Asaka
authors.forename: Junko
authors.initials: J
authors.lastname: Akaishi
authors.forename: Shizuyo
authors.initials: S
authors.lastname: Miyamoto
authors.forename: Akira
authors.initials: A
authors.lastname: Yoshida
authors.forename: Mitsuji
authors.initials: M
authors.lastname: Nagahama
authors.forename: Kouichi
authors.initials: K
authors.lastname: Ito
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Emi
mesh_terms: D002277:Carcinoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D049109:Cell Proliferation; D004268:DNA-Binding Proteins; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D006801:Humans; D046228:Microarray Analysis; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013961:Thyroid Gland / Q000378:metabolism / Q000473:pathology; D013964:Thyroid Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D014162:Transfection; D014407:Tumor Cells, Cultured
chemical_list: D002352:Carrier Proteins; D004268:DNA-Binding Proteins; C425208:PCLAF protein, human; D012333:RNA, Messenger; D034741:RNA, Small Interfering