title: 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.
abstract: 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.
authors.affiliation: Palladin Institute of Biochemistry, National Academy of Science of Ukraine, Kyiv. ominchenko@yahoo.com
authors.forename: D O
authors.initials: DO
authors.lastname: Minchenko
authors.forename: O V
authors.initials: OV
authors.lastname: Hubenya
authors.forename: B M
authors.initials: BM
authors.lastname: Terletsky
authors.forename: M
authors.initials: M
authors.lastname: Moenner
authors.forename: O H
authors.initials: OH
authors.lastname: Minchenko
mesh_terms: D018929:Cell Culture Techniques; D045744:Cell Line, Tumor; D003001:Cloning, Molecular; D003470:Culture Media; D018844:Cyclin-Dependent Kinases / Q000037:antagonists & inhibitors / Q000235:genetics*; D016213:Cyclins / Q000235:genetics*; D004721:Endoplasmic Reticulum / Q000201:enzymology / Q000378:metabolism; D004722:Endoribonucleases / Q000037:antagonists & inhibitors* / Q000235:genetics; D005910:Glioma / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D005947:Glucose / Q000172:deficiency* / Q000494:pharmacology; D005973:Glutamine / Q000172:deficiency* / Q000494:pharmacology; D006801:Humans; D007511:Ischemia / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors* / Q000235:genetics; D058767:Protein Unfolding; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014162:Transfection
chemical_list: D003470:Culture Media; D016213:Cyclins; D005973:Glutamine; C528229:ERN1 protein, human; D017346:Protein Serine-Threonine Kinases; D018844:Cyclin-Dependent Kinases; D004722:Endoribonucleases; D005947:Glucose