title: Hyper-expression of PAX2 in human metastatic prostate tumors and its role as a cancer promoter in an in vitro invasion model.
abstract: BACKGROUND
  Metastasis is a consequence of many biological events, during which cancer stem cells are shifted into a malignant state. Among these events, invasion of prostate cancer cells into host tissues is possible to be assessed by means of an in vitro invasion model, and is thought to be coupled to altered expression of membrane proteins. Dysregulated functions of the factors regulating organogenesis during embryogenesis are known to facilitate metastasis of many types of cancers. PAX2 (paired box 2) is a member of the PAX transcription factor family, which regulates prostatic ductal growth and branching in organogenesis of mammalian prostates. However, the role of PAX2 in prostate cancer development remains to be determined.
  
  
  METHODS
  PAX2 expression in human prostate cancers and normal prostate epithelium were examined by quantitative RT-PCR and immunohistochemistry. Matrigel invasion assay and a gene array analysis were performed using prostate cancer cell lines transfected with either control or PAX2 siRNA.
  
  
  RESULTS
  In human prostate cancers, PAX2 was hyper-expressed in metastatic cancers, but was expressed at lower levels in non-metastatic cancers. Consistent with this, PAX2 knockdown repressed cell growth and invasion in a Matrigel invasion assay. Gene ontology analysis revealed that many cell membrane proteins were downregulated after PAX2 knockdown.
  
  
  CONCLUSIONS
  Our data suggested that PAX2 hyper-expression promotes the development of the metastatic state in prostate cancer cells, presumably through upregulating the expression of cell membrane proteins.
authors.affiliation: Department of Urology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan. t-ueda@koto.kpu-m.ac.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Ueda
authors.forename: Saya
authors.initials: S
authors.lastname: Ito
authors.forename: Takumi
authors.initials: T
authors.lastname: Shiraishi
authors.forename: Prakash
authors.initials: P
authors.lastname: Kulkarni
authors.forename: Akihisa
authors.initials: A
authors.lastname: Ueno
authors.forename: Hideo
authors.initials: H
authors.lastname: Nakagawa
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Kimura
authors.forename: Fumiya
authors.initials: F
authors.lastname: Hongo
authors.forename: Kazumi
authors.initials: K
authors.lastname: Kamoi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Kawauchi
authors.forename: Tsuneharu
authors.initials: T
authors.lastname: Miki
mesh_terms: D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D009362:Neoplasm Metastasis / Q000235:genetics* / Q000473:pathology; D051762:PAX2 Transcription Factor / Q000235:genetics* / Q000378:metabolism; D011467:Prostate / Q000378:metabolism* / Q000473:pathology; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D015854:Up-Regulation
chemical_list: D051762:PAX2 Transcription Factor; C497318:PAX2 protein, human
keywords: PAX2; invasion; membrane protein; metastasis; prostate cancer