Biopolym. Cell. 2015; 31(4):316-320.
Short Communications
Glioma-associated protein CHI3L2 suppresses cells viability and induces G1/S transition arrest
1Avdieiev S. S., 2Gera L., 2Hodges R., 1Dmytrenko V. V.
  1. Institute of Molecular Biology and Genetics, NAS of Ukraine
    150, Akademika Zabolotnoho Str., Kyiv, Ukraine, 03680
  2. Department of Biochemistry and Molecular Genetics, University of Colorado Denver
    Anschutz Medical Campus, Aurora CO 80045, USA

Abstract

Aim. To analyze the effect of the CHI3L2 protein on malignant and non-malignant cell viability, and determined the CHI3L2 impact on the cell cycle and signaling pathways involved in the cell cycle regulation. Methods. MTT-based cell proliferation assay, FACS, western blot analysis. Results. The CHI3L2 protein inhibits the glioma cells viability and potentiates the effect of anti-cancer cytotoxic agents. The CHI3L2 treatment results in the G1/S transition arrest. CHI3L2 provoked a dramatic reduction of pRB phosphorylation and a significant decrease in the cyclin D1 expression, whereas the p53 and p21 expression levels were substantially increased. Conclusions. The CHI3L2 protein, which is overexpressed in human gliomas, is a negative regulator of the glioma cells viability. The reduced cell viability after the CHI3L2 treatment could be due to the activation of pRB and p53 and the downregulation of cyclin D.
Keywords: chitinase-like proteins, glioma, bradykinin antagonists, signaling cascades., cell cycle

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