title: Surface CD24 distinguishes between low differentiated and transit-amplifying cells in the basal layer of human prostate.
abstract: BACKGROUND
  Benign prostatic hyperplasia (BPH) and prostate cancer (PCa) are common abnormalities in elderly men. It is considered that epithelial stem cells are involved in the etiology and development of both diseases. To distinguish aberrant from normal cells, the knowledge about primary epithelial stem/progenitor cells (ES/P) is essential. The aim of this study was to examine the role of surface markers to distinguish between different subsets of prostate basal epithelium.
  
  
  METHODS
  The expression pattern of prostate tissue single cell suspensions was analyzed by flow cytometry using different markers. Sorted cell populations were examined for their clonogenic capacity and the resulted colonies were analyzed with flow cytometry, Western blot, and qPCR for stem cell, basal, and luminal epithelium markers. Additionally, the histological localization of the examined markers was determined using immunofluorescence.
  
  
  RESULTS
  Using the combination of CD49f, Trop-2, and surface CD24, basal cell subsets with distinct differentiation capacities were dissected (CD49f(+) Trop-2(+) CD24(-) and CD49f(+) Trop-2(+) CD24(+) ). Although cells from the two subsets gave rise to similar basal colonies, qPCR of primary tissue revealed that higher levels of basal marker expression were detected in the CD49f(+) Trop-2(+) CD24(-) subset. Immunofluorescence analysis showed a prominent expression of CD24 by luminal and basal cells.
  
  
  CONCLUSIONS
  Subsets with distinct differentiation capacities within the basal epithelium (CD49f(+) Trop-2(+) CD24(-) and CD49f(+) Trop-2(+) CD24(+) ) can be distinguished in human prostate. CD24 is a marker expressed on the basal transit-amplifying cells (transition cells) and may play a role in the differentiation and migration of ES/P cells to the luminal layer. The knowledge of this mechanism is of relevance for treatment of both diseases.
authors.affiliation: Department of Urology, University Hospital Tuebingen, Tuebingen, Germany.
authors.forename: Neli
authors.initials: N
authors.lastname: Petkova
authors.forename: Jörg
authors.initials: J
authors.lastname: Hennenlotter
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Sobiesiak
authors.forename: Tilman
authors.initials: T
authors.lastname: Todenhöfer
authors.forename: Marcus
authors.initials: M
authors.lastname: Scharpf
authors.forename: Arnulf
authors.initials: A
authors.lastname: Stenzl
authors.forename: Hans-Jörg
authors.initials: HJ
authors.lastname: Bühring
authors.forename: Christian
authors.initials: C
authors.lastname: Schwentner
mesh_terms: D000368:Aged; D000943:Antigens, Differentiation; D000954:Antigens, Surface / Q000235:genetics / Q000378:metabolism; D051927:CD24 Antigen / Q000235:genetics / Q000378:metabolism; D002465:Cell Movement; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D039503:Integrin alpha6 / Q000378:metabolism; D008297:Male; D011467:Prostate / Q000378:metabolism / Q000473:pathology*; D011470:Prostatic Hyperplasia / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology
chemical_list: D000943:Antigens, Differentiation; D000954:Antigens, Surface; D051927:CD24 Antigen; D039503:Integrin alpha6
keywords: CD24; benign prostatic hyperplasia; prostate differentiation; prostate stem cells; prostate transit-amplifying cells