title: Aberrant expression of katanin p60 in prostate cancer bone metastasis.
abstract: BACKGROUND
  Katanin p60 is a microtubule-severing protein and is involved in microtubule cytoskeleton organization in both mitotic and non-mitotic processes. Its role in cancer metastasis is unknown.
  
  
  METHODS
  Differential protein profiles of bone marrow aspirates were analyzed by chromatography, electrophoresis, and mass spectrometry. Expression of katanin p60 in primary and metastatic prostate cancer was examined by immunohistochemistry. Cellular function of katanin p60 was further examined in prostate cell lines.
  
  
  RESULTS
  In a proteomic profiling of bone marrow aspirates from men with prostate cancer, we found that katanin p60 was one of the proteins differentially expressed in bone metastasis samples. Immunohistochemical staining showed that katanin p60 was expressed in the basal cells in normal human prostate glands. In prostatic adenocarcinomas, in which the basal cells were absent, katanin p60 was expressed in the prostate cancer cells. In the specimens from bone metastasis, katanin p60 was detectable in the metastatic cancer cells. Strikingly, some of the metastatic cancer cells also co-expressed basal cell biomarkers including the tumor suppressor p53-homologous protein p63 and the high molecular weight cytokeratins, suggesting that the metastatic prostate cancer cells may have a basal cell-like phenotype. Moreover, overexpression of katanin p60 inhibited prostate cancer cell proliferation but enhanced cell migration activity.
  
  
  CONCLUSIONS
  Katanin p60 was aberrantly expressed during prostate cancer progression. Its expression in the metastatic cells in bone was associated with the re-emergence of a basal cell-like phenotype. The elevated katanin p60 expression may contribute to cancer cell metastasis via a stimulatory effect on cell motility.
authors.affiliation: Department of Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. xcye@mdanderson.org
authors.forename: Xiangcang
authors.initials: X
authors.lastname: Ye
authors.forename: Yu-Chen
authors.initials: YC
authors.lastname: Lee
authors.forename: Michel
authors.initials: M
authors.lastname: Choueiri
authors.forename: Khoi
authors.initials: K
authors.lastname: Chu
authors.forename: Chih-Fen
authors.initials: CF
authors.lastname: Huang
authors.forename: Wen-Wei
authors.initials: WW
authors.lastname: Tsai
authors.forename: Ryuji
authors.initials: R
authors.lastname: Kobayashi
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Logothetis
authors.forename: Li-Yuan
authors.initials: LY
authors.lastname: Yu-Lee
authors.forename: Sue-Hwa
authors.initials: SH
authors.lastname: Lin
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000503:physiopathology / Q000556:secondary*; D000251:Adenosine Triphosphatases / Q000378:metabolism*; D014408:Biomarkers, Tumor / Q000378:metabolism; D001706:Biopsy; D001853:Bone Marrow / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001859:Bone Neoplasms / Q000378:metabolism* / Q000503:physiopathology / Q000556:secondary*; D002465:Cell Movement / Q000502:physiology; D049109:Cell Proliferation; D006801:Humans; D000074201:Katanin; D008297:Male; D008875:Middle Aged; D011467:Prostate / Q000378:metabolism / Q000473:pathology; D011471:Prostatic Neoplasms / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D012189:Retrospective Studies; D015854:Up-Regulation
chemical_list: D014408:Biomarkers, Tumor; D000251:Adenosine Triphosphatases; C570385:KATNA1 protein, human; D000074201:Katanin