title: Expression profiling of PC-3 cell line variants and comparison of MIC-1 transcript levels in benign and malignant prostate.
abstract: BACKGROUND
  The mechanisms behind prostate cancer progression are largely unknown, but macrophage inhibitory cytokine 1 (MIC-1) has been suggested to be involved in tumour dissemination in vivo due to its reductive effect on cell adhesion.
  
  
  METHODS
  We used two PC-3 prostate cancer epithelial cell line variants as tools to screen for gene expression differences during prostate cancer progression by cDNA microarray analysis. Selected genes were further analysed by Northern blot analysis using mRNA isolated from prostatic cell lines and tissues. MIC-1 expression was studied by in situ hybridization in archival patient specimens containing benign and malignant prostatic tissue.
  
  
  RESULTS
  Gene expression of human collagen type VI, basement membrane heparan sulphate proteoglycan, integrin alpha 1, and fibronectin I were remarkably decreased in suspension-adapted PC-3 (saPC-3) cells, indicating a gene expression profile of reduced cell adhesion. Asparagine synthetase, serine protease 1, stanniocalcin homologue, NAD-dependent methylene tetrahydrate dehydrogenase cyclohydrolase (NMDMC), fortilin, and MIC-1 were overexpressed in saPC-3 cells. In prostate, the MIC-1 gene was mainly expressed in cancer tissue. However, MIC-1 transcripts were detected in benign tissue areas, especially in specimens containing prostate cancer with Gleason sum scores of 5-8. A significant inverse correlation (Spearman's rho correlation coefficient -0.928**) was observed between the ratio of cancerous to benign MIC-1 expression levels and Gleason scores.
  
  
  CONCLUSIONS
  Differential expression of the MIC-1 gene occurs during prostate cancer progression. The transcript level of the MIC-1 gene in histologically benign tissue seems to approach that in paired cancer tissue concomitant with an increasing Gleason score.
authors.affiliation: WHO Collaborating Centre for Research on Reproductive Health University of Oulu, Finland.
authors.forename: L
authors.initials: L
authors.lastname: Patrikainen
authors.forename: K
authors.initials: K
authors.lastname: Porvari
authors.forename: R
authors.initials: R
authors.lastname: Kurkela
authors.forename: P
authors.initials: P
authors.lastname: Hirvikoski
authors.forename: Y
authors.initials: Y
authors.lastname: Soini
authors.forename: P
authors.initials: P
authors.lastname: Vihko
mesh_terms: D015152:Blotting, Northern; D002448:Cell Adhesion / Q000502:physiology; D045744:Cell Line, Tumor; D016207:Cytokines / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism; D015870:Gene Expression; D055436:Growth Differentiation Factor 15; D006801:Humans; D008297:Male; D011471:Prostatic Neoplasms / Q000175:diagnosis*; D012333:RNA, Messenger / Q000378:metabolism
chemical_list: D016207:Cytokines; C526140:GDF15 protein, human; D055436:Growth Differentiation Factor 15; D012333:RNA, Messenger