title: The human RECQ1 helicase is highly expressed in glioblastoma and plays an important role in tumor cell proliferation.
abstract: BACKGROUND
  RecQ helicases play an essential role in the maintenance of genome stability. In humans, loss of RecQ helicase function is linked with predisposition to cancer and/or premature ageing. Current data show that the specific depletion of the human RECQ1 helicase leads to mitotic catastrophe in cancer cells and inhibition of tumor growth in mice.
  
  
  RESULTS
  Here, we show that RECQ1 is highly expressed in various types of solid tumors. However, only in the case of brain gliomas, the high expression of RECQ1 in glioblastoma tissues is paralleled by a lower expression in the control samples due to the poor expression of RECQ1 in non-dividing tissues. This conclusion is validated by immunohistochemical analysis of a tissue microarray containing 63 primary glioblastomas and 19 perilesional tissue samples, as control. We also show that acute depletion of RECQ1 by RNAi results in a significant reduction of cellular proliferation, perturbation of S-phase progression, and spontaneous γ-H2AX foci formation in T98G and U-87 glioblastoma cells. Moreover, RECQ1 depleted T98G and U-87 cells are hypersensitive to HU or temozolomide treatment.
  
  
  CONCLUSIONS
  Collectively, these results indicate that RECQ1 has a unique and important role in the maintenance of genome integrity. Our results also suggest that RECQ1 might represent a new suitable target for anti cancer therapies aimed to arrest cell proliferation in brain gliomas.
authors.affiliation: International Centre for Genetic Engineering and Biotechnology Padriciano 99, 34149 Trieste, Italy. mendoza@icgeb.org
authors.forename: Ramiro
authors.initials: R
authors.lastname: Mendoza-Maldonado
authors.forename: Valentina
authors.initials: V
authors.lastname: Faoro
authors.forename: Sailesh
authors.initials: S
authors.lastname: Bajpai
authors.forename: Matteo
authors.initials: M
authors.lastname: Berti
authors.forename: Federico
authors.initials: F
authors.lastname: Odreman
authors.forename: Marco
authors.initials: M
authors.lastname: Vindigni
authors.forename: Tamara
authors.initials: T
authors.lastname: Ius
authors.forename: Abdollah
authors.initials: A
authors.lastname: Ghasemian
authors.forename: Serena
authors.initials: S
authors.lastname: Bonin
authors.forename: Miran
authors.initials: M
authors.lastname: Skrap
authors.forename: Giorgio
authors.initials: G
authors.lastname: Stanta
authors.forename: Alessandro
authors.initials: A
authors.lastname: Vindigni
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D001932:Brain Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects / Q000502:physiology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects / Q000502:physiology; D005909:Glioblastoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008297:Male; D051379:Mice; D008875:Middle Aged; D034741:RNA, Small Interfering / Q000494:pharmacology; D053484:RecQ Helicases / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism / Q000502:physiology*; D047368:Tumor Burden / Q000187:drug effects / Q000235:genetics*; D015854:Up-Regulation / Q000187:drug effects / Q000235:genetics
chemical_list: D034741:RNA, Small Interfering; C506725:RECQL protein, human; D053484:RecQ Helicases