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Microtubule-severing ATPase spastin in glioblastoma: increased expression in human glioblastoma cell lines and inverse roles in cell motility and proliferation

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    0365459 - ÚMG 2012 RIV US eng J - Journal Article
    Dráberová, Eduarda - Vinopal, Stanislav - Morfini, G. - Liu, P. S. - Sládková, Vladimíra - Sulimenko, Tetyana - Burns, M.R. - Solowska, J. - Kulandaivel, K. - De Chadarévian, J.P. - Legido, A. - Mork, S.J. - Janáček, Jiří - Baas, P. - Dráber, Pavel - Katsetos, C.D.
    Microtubule-severing ATPase spastin in glioblastoma: increased expression in human glioblastoma cell lines and inverse roles in cell motility and proliferation.
    Journal of Neuropathology and Experimental Neurology. Roč. 70, č. 9 (2011), s. 811-826. ISSN 0022-3069. E-ISSN 1554-6578
    R&D Projects: GA ČR GAP302/10/1701; GA ČR GA204/09/1777; GA ČR(CZ) GD204/09/H084; GA AV ČR KAN200520701; GA MŠMT LC545
    Institutional research plan: CEZ:AV0Z50520514; CEZ:AV0Z50110509
    Keywords : spastin * glioblastoma * cell motility
    Subject RIV: EB - Genetics ; Molecular Biology
    Impact factor: 4.258, year: 2011

    This research article is first report of the role of spastin in cell motility. The enzyme spastin is from microtubule-severing ATPases and regulates lenght of microtubules. Among strategies used for treating malignant tumors belongs disrupting the integrity of microtubules. The role of microtubules on invasivity has the higher propensity especially in glioblastoma cells from brain. To find the answer to question, if spastin and microtubules regulation somehow influence each other, spastin expression evaluation and testing of intracellular distribution was performed in human glioblastomas and astrocytes. It was found that spastin expression is increased in tumor cells. Surprisingly, functional experiments comparing the effects of spastin depletion on the motility and proliferation in glioblastomas have shown decreased motility and higher proliferation rate. The article proposes that spastin in glioblastomas might be linked to tumor cell invasion.
    Permanent Link: http://hdl.handle.net/11104/0200696

     
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