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• W2891692332 abstract "// Ramon Martinez-Olivera 1, * , Angeliki Datsi 2, 3, * , Maren Stallkamp 2, 4 , Manfred Köller 5 , Isabelle Kohtz 2 , Bogdan Pintea 1 and Konstantinos Gousias 1, 2, 4, 6 1 Department of Neurosurgery and Neurotraumatology, BG University Hospital Bergmannsheil, 44789 Bochum, Germany 2 Department of Laboratory for Neurosurgical Research, BG University Hospital Bergmannsheil, 44789 Bochum, Germany 3 Institute for Transplantation Diagnostics and Cell Therapeutics, Heinrich-Heine University, 40225 Düsseldorf, Germany 4 Medical School, Rheinische Friedrich-Wilhelms University of Bonn, 53121 Bonn, Germany 5 Department of Surgical Research, BG University Hospital Bergmannsheil, 44789 Bochum, Germany 6 Department of Neurosurgery, University Hospital of Marburg, 35033 Marburg, Germany * These authors contributed equally to this work Correspondence to: Konstantinos Gousias, email: kostasgousias@yahoo.com Keywords: glioblastoma multiforme; karyopherin a2; U87 MG; nucleocytoplasmic transport Received: December 13, 2017      Accepted: August 04, 2018      Published: September 11, 2018 ABSTRACT We have previously shown that the nucleocytoplasmic carrier karyopherin a2 (KPNA2) is overexpressed in glioblastoma multiforme (GBM) whereas its expression is inversely associated with patient prognosis. However, the promoting role of KPNA2 in gliomagenesis is still poorly understood. This study aims to further elucidate this role of KPNA2 in in vitro GBM models. From four different tested GBM cell lines, the U87MG showed the highest proliferation, low adherence and outgrowth in 3D clusters as well as the highest expression of KPNA2, all features conferring greater malignant behaviour. Silencing of KPNA2 via siRNA interference in those cells significantly decreased their proliferative capacity ( p = 0.001). We further observed both a significant cell cycle phase arrest ( p = 0.040) and the promoting of cellular apoptosis ( p = 0.016) as well as a strong trend ( p = 0.062) for an inhibition of nuclear import of c-Myc. This study confirms that a higher expression of KPNA2 in GBM is associated with a more malignant phenotype also in in vitro models. While increased expression of KPNA2 promotes proliferation and survival of GBM tumour cells, silencing of KPNA2 conferred a less malignant behaviour. Our results strongly suggest that silencing of KPNA2 may play an important role in modulation of malignant features of GBM cells." @default.
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• W2891692332 date "2018-09-11" @default.
• W2891692332 modified "2023-09-26" @default.
• W2891692332 title "Silencing of the nucleocytoplasmic shuttling protein karyopherin a2 promotes cell-cycle arrest and apoptosis in glioblastoma multiforme" @default.
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• W2891692332 doi "https://doi.org/10.18632/oncotarget.26033" @default.
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