EGFR involvement in neural and mesenchymal differentiation of glioblastoma progenitor cells

• Autorzy: Rieske P. , Witusik P. , Golanska E. , Piaskowski S. , Zakrzewski M. , Gresner S. , Jaskolski D.J. , Zakrzewski K. , Wolanczyk M. , Krynska B. , Hulas-Bigoszewska K. , Szybka M. , Kulczycka-Wojdala D. , Liberski P.P.
• Języki publikacji: EN

Abstrakty

EN

We have compared differentiation ability of glioblastoma cells with differentiation ability of neural progenitors. An effi cient differentiation arrest was observed in all cell lines isolated from glioblastomas in contrast to normal neural progenitors. However, cells isolated from six glioblastomas showed features of early stages of neural differentiation. Moreover, the cells derived from a majority of glioblastomas (8 out of 10) as well as neural progenitors showed features of non-neural (mesenchymal-like) differentiation. Moreover aggregated cells sustained EGFR amplifi cation, whereas cells grown as a monolayer did not. Cells showing EGFR amplifi cation became apoptotic grown as monolayer. Majority of mesenchymally differentiated glioblastoma cells showed features of senescence. Novel hypotheses which we would like to test are as follows: Neural progenitors could be a potential source of glioblastomas. Glioblastoma presents not only tumor stem cells but also tumor progenitor cells. Stable coexpression of glial and neuronal markers presented by glioblastoma cells results from differentiation arrest. Aggregating glioblastoma cells allows to sustain, EGFR amplifi cation in vitro. Moreover aggregated cells show proliferation ability, and differentiation arrest, whereas monolayer cells can be effi ciently differentiated and fi nally senescent. It suggests that simultaneous analysis of differentiation processes altogether with considering status of genes such as EGFR may help in designing new molecular targets for chemotherapy.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2009
• Tom: 69
• Numer: 1
• Opis fizyczny: p.108

Twórcy

autor

Rieske P.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland

autor

Witusik P.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland

autor

Golanska E.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland

autor

Piaskowski S.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland

autor

Zakrzewski M.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland

autor

Gresner S.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland

autor

Jaskolski D.J.

• Department of Neurosurgery, Medical University of Lodz, Lodz, Poland

autor

Zakrzewski K.

• Chair of Pediatric Neurosurgery and Neurology, Department of Pediatric Neurosurgery, Medical University of Lodz, Lodz, Poland;

autor

Wolanczyk M.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland

autor

Krynska B.

• Chair of Oncology, Department of Oncological Pathology, Medical University of Lodz, Lodz, Poland

autor

Hulas-Bigoszewska K.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland

autor

Szybka M.

• Department of Neurology, Temple University, USA

autor

Kulczycka-Wojdala D.

• Department of Neurology, Temple University, USA

autor

Liberski P.P.

• Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Lodz, Poland