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Signal transduction molecule patterns indicating potential glioblastoma therapy approaches

Authors Cruceru ML, Enciu A, Popa A, Albulescu R, Neagu M, Tanase C, Constantinescu SN

Received 2 August 2013

Accepted for publication 4 October 2013

Published 29 November 2013 Volume 2013:6 Pages 1737—1749

DOI https://doi.org/10.2147/OTT.S52365

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

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Maria Linda Cruceru,1 Ana-Maria Enciu,1,2,7 Adrian Claudiu Popa,1,3 Radu Albulescu,2,4,7 Monica Neagu,2,7 Cristiana Pistol Tanase,2,7 Stefan N Constantinescu5–7

1Carol Davila University of Medicine and Pharmacy, Department of Cellular and Molecular Medicine, Bucharest, Romania; 2Victor Babes National Institute of Pathology, Bucharest, Romania; 3Army Centre for Medical Research, Bucharest, Romania; 4National Institute for Chemical Pharmaceutical R&D, Bucharest, Romania; 5de Duve Institute, Université Catholique de Louvain, Brussels, Belgium; 6Ludwig Institute for Cancer Research, Brussels, Belgium; 7Operational Sectorial Programme for Competitive Economic Growth Canbioprot at Victor Babes National Institute of Pathology, Bucharest, Romania

Purpose: The expression of an array of signaling molecules, along with the assessment of real-time cell proliferation, has been performed in U87 glioma cell line and in patients’ glioblastoma established cell cultures in order to provide a better understanding of cellular and molecular events involved in glioblastoma pathogenesis. Experimental therapy was performed using a phosphatydylinositol-3´-kinase (PI3K) inhibitor.
Patients and methods: xMAP technology was employed to assess expression levels of several signal transduction molecules and real-time xCELLigence platform for cell behavior.
Results: PI3K inhibition induced the most significant effects on global signaling pathways in patient-derived cell cultures, especially on members of the mitogen-activated protein-kinase family, P70S6 serine-threonine kinase, and cAMP response element-binding protein expression and further prevented tumor cell proliferation.
Conclusion: The PI3K pathway might be a prime target for glioblastoma treatment.

Keywords: personalized medicine, PI3K inhibitor, targeted therapy, xCELLigence, xMAP analysis

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