title: Upregulation of the cycline kinase subunit CKS2 increases cell proliferation rate in gastric cancer.
abstract: OBJECTIVE
  CKS2 was identified as an upregulated gene in gastric cancer via our DNA microarray. This study was to verify the upregulation of CKS2 in many gastric cancer patients and to examine the CKS2-mediated cellular response.
  
  
  METHODS
  CKS2 upregulation was analyzed using reverse transcriptase PCR, real-time PCR, and immunohistochemical and clinicopathological analyses. GFP-CKS2 or CKS2-siRNA was used to analyze the cellular localization and proliferation.
  
  
  RESULTS
  The strong upregulation of mRNA and protein levels of CKS2 was identified. In CKS2-overexpressing cells, tumor suppressor p53 and p21(cip1) were downregulated and cell growth was increased. In contrast, CKS2-siRNA-transfected cells showed an increased tumor suppressor expression and decreased cell growth.
  
  
  CONCLUSIONS
  We showed that CKS2 was significantly upregulated in gastric cancers and a high level of CKS2 was highly correlated with histologic tumor differentiation and pathological grade of the tumor size, lymph node, and metastasis stage. We suggest that the cell cycle regulator CKS2 might be deeply involved in gastric cancer progression.
authors.affiliation: Stem Cell Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
authors.forename: Min Ah
authors.initials: MA
authors.lastname: Kang
authors.forename: Jong-Tae
authors.initials: JT
authors.lastname: Kim
authors.forename: Joo Heon
authors.initials: JH
authors.lastname: Kim
authors.forename: Soo-Young
authors.initials: SY
authors.lastname: Kim
authors.forename: Young Ho
authors.initials: YH
authors.lastname: Kim
authors.forename: Young Il
authors.initials: YI
authors.lastname: Yeom
authors.forename: Younghee
authors.initials: Y
authors.lastname: Lee
authors.forename: Hee Gu
authors.initials: HG
authors.lastname: Lee
mesh_terms: D015153:Blotting, Western; D042846:CDC2-CDC28 Kinases; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D018797:Cell Cycle Proteins / Q000235:genetics* / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D018613:Microscopy, Confocal; D008875:Middle Aged; D011494:Protein Kinases / Q000235:genetics* / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013274:Stomach Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D014158:Transcription, Genetic; D014162:Transfection; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D002352:Carrier Proteins; D018797:Cell Cycle Proteins; D034741:RNA, Small Interfering; D011993:Recombinant Fusion Proteins; D016159:Tumor Suppressor Protein p53; D049452:Green Fluorescent Proteins; D011494:Protein Kinases; D042846:CDC2-CDC28 Kinases; C083689:CKS2 protein, human