Journal archive > 2011 > N 1 January-February

EFFECT OF GLUTAMINE OR GLUCOSE DEPRIVATION ON THE EXPRESSION OF CYCLIN
AND CYCLIN-DEPENDENT KINASE GENES IN GLIOMA CELL LINE U87 AND ITS SUBLINE
WITH SUPPRESSED ACTIVITY OF SIGNALING ENZYME OF ENDOPLASMIC RETICULUM–NUCLEI-1

D. O. Minchenko1,2,3, O. V. Hubenya1, B. M. Terletsky1, M. Moenner3, O. H. Minchenko1,3

1Palladin Institute of Biochemistry, National Academy of Science of Ukraine, Kyiv;
e-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.;
2National O. O. Bohomoletz Medical University, Kyiv, Ukraine;
3INSERM U920 Molecular Mechanisms of Angiogenesis Laboratory,
University Bordeaux 1, Talence, France

Ischemia has been shown to induce a set of complex intracellular signaling events known as the unfolded protein response, which is mediated by endoplasmic reticulum–nuclei-1 sensing enzyme. We have studied the expression of several cyclin and cyclin-dependent kinase genes which participate in the control of cell cycle and proliferation under ischemic conditions (glucose or glutamine deprivation) in endoplasmic reticulum–nuc­lei?1-deficient glioma cells. It was shown that blockade of endoplasmic reticulum–nuclei signaling enzyme-1, the key endoplasmic reticulum stress sensor, leads to an increase of the expression levels of cyclin-dependent kinase-2 and cyclin A2, D3, E2 and G2 genes but suppresses cyclin D1. Moreover, the expression level of cyclin-dependent kinase-2 as well as cyclin A2, D3 and E2 mRNAs is significantly decreased under glucose or glutamine deprivation conditions both in control and endoplasmic reticulum–nuclei-1-deficient glioma cells. However, cyclin-dependent kinase-4 and -5 mRNA expressions is increased, but in glucose deprivation conditions only.  Results of this study have shown that the expression of most tested genes of encoded cyclins and cyclin-dependent kinases is dependent on endoplasmic reticulum–nuclei-1 signaling enzyme function both in normal and glutamine and glucose deprivation conditions and possibly participates in cell adaptive response to endoplasmic reticulum stress associated with ischemia.

Key words: mRNA expression, cyclin A2, D1, D3, E2 and G2, cyclin-dependent kinase-2, -4 and -5, glioma cells, endoplasmic reticulum–nuclei-1, glucose and glutamine deprivation.

The original article in English is available for download in PDF format.

 

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