title: CIP2A is overexpressed in non-small cell lung cancer and correlates with poor prognosis.
abstract: BACKGROUND
  Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an oncoprotein inhibiting proteolytic degradation of c-MYC. In this study, we investigated the clinical relevance of CIP2A in NSCLC.
  
  
  METHODS
  We analyzed CIP2A mRNA expression in 29 NSCLC tissues using quantitative reverse transcription polymerase chain reaction (RT-QPCR). We also examined the expression of CIP2A protein by immunohistochemistry in 90 lung cancer specimens and correlated its expression with c-MYC expression and clinicopathological parameters. The functional roles of CIP2A in lung cancer cell lines were evaluated by small interfering RNA-mediated depletion of the protein followed by analyses of cell proliferation and invasion.
  
  
  RESULTS
  In 29 lung cancer tissues examined, 24 of them (82.7%) exhibited much stronger levels of CIP2A mRNA compared with their corresponding normal tissues. Moreover, CIP2A mRNA expression levels correlated with c-MYC mRNA levels. Furthermore, CIP2A protein was found to be overexpressed in 72.2% of 90 human lung cancer samples and correlated with poor survival (P < 0.05). In addition, the CIP2A status was a significant prognostic factor for NSCLC patients (P = 0.0136). Depleting CIP2A expression inhibited growth and clonogenic potential in lung cancer cell lines.
  
  
  CONCLUSIONS
  CIP2A is an oncoprotein overexpressed in NSCLC, and its expression is associated with poor prognosis and malignant cell proliferation.
authors.affiliation: Department of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences of China Medical University, Shenyang, China.
authors.forename: Qian-Ze
authors.initials: QZ
authors.lastname: Dong
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Xin-Jun
authors.initials: XJ
authors.lastname: Dong
authors.forename: Zi-Xuan
authors.initials: ZX
authors.lastname: Li
authors.forename: Zhong-Ping
authors.initials: ZP
authors.lastname: Tang
authors.forename: Quan-Ze
authors.initials: QZ
authors.lastname: Cui
authors.forename: En-Hua
authors.initials: EH
authors.lastname: Wang
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D001324:Autoantigens / Q000235:genetics* / Q000378:metabolism; D015153:Blotting, Western; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002448:Cell Adhesion; D002465:Cell Movement; D049109:Cell Proliferation; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D047908:Intracellular Signaling Peptides and Proteins; D008175:Lung Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008565:Membrane Proteins / Q000235:genetics* / Q000378:metabolism; D008875:Middle Aged; D011379:Prognosis; D016271:Proto-Oncogene Proteins c-myc; D012333:RNA, Messenger / Q000235:genetics; D034741:RNA, Small Interfering / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015996:Survival Rate; D014407:Tumor Cells, Cultured
chemical_list: D001324:Autoantigens; C500266:CIP2A protein, human; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D016271:Proto-Oncogene Proteins c-myc; D012333:RNA, Messenger; D034741:RNA, Small Interfering