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4 results on '"glucose and glutamine deprivations"'

1. ERN1 dependent impact of glucose and glutamine deprivations on PBX3, PBXIP1, PAX6, MEIS1, and MEIS2 genes expression in U87 glioma cells

Author

Krasnytska Dariia O., Viletska Yuliia M., Minchenko Dmytro O., Khita Olena O., Tsymbal Dariia O., Cherednychenko Anastasiia A., Kozynkevych Halyna E., Oksiom Nataliia S., and Minchenko Oleksandr H.

Subjects
u87 glioma cells, ern1 knockdown, glucose and glutamine deprivations, homeobox genes, mrna expression, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

Objective. Homeobox genes play a fundamental role in the embryogenesis, but some of them have been linked to oncogenesis. The present study is aimed to investigate the impact of glucose and glutamine deprivations on the expression of homeobox genes such as PAX6 (paired box 6), PBX3 (PBX homeobox 3), PBXIP1 (PBX homeobox interacting protein 1), MEIS1 (MEIS homeobox 1), and MEIS2 in ERN1 knockdown U87 glioma cells with the intent to reveal the role of ERN1 (endoplasmic reticulum to nucleus signaling 1) signaling pathway on the endoplasmic reticulum stress dependent regulation of homeobox genes.

Published
2023
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2. ERN1 knockdown modifies the impact of glucose and glutamine deprivations on the expression of EDN1 and its receptors in glioma cells

Author

Minchenko Dmytro O., Khita Olena O., Tsymbal Dariia O., Viletska Yuliia M., Sliusar Myroslava Y., Yefimova Yuliia V., Levadna Liudmyla O., Krasnytska Dariia A., and Minchenko Oleksandr H.

Subjects
ern1 knockdown, mrna expression, edn1, ednra, ednrb, ece1, glucose and glutamine deprivations, u87 glioma cells, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

Objective. The aim of the present investigation was to study the impact of glucose and gluta-mine deprivations on the expression of genes encoding EDN1 (endothelin-1), its cognate receptors (EDNRA and EDNRB), and ECE1 (endothelin converting enzyme 1) in U87 glioma cells in response to knockdown of ERN1 (endoplasmic reticulum to nucleus signaling 1), a major signaling pathway of endoplasmic reticulum stress, for evaluation of their possible implication in the control of glioma growth through ERN1 and nutrient limitations.

Published
2021
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3. IRE1 KNOCKDOWN MODIFIES THE GLUTAMINE AND GLUCOSE DEPRIVATION EFFECT ON THE EXPRESSION OF NUCLEAR GENES ENCODING MITOCHONDRIAL PROTEINS IN U87 GLIOMA CELLS

Author

O. O., D. O., O.O., and O. H.

Subjects
glucose and glutamine deprivations, mitochondrial proteins, IRE1 inhibition, U87 glioma cells., Biotechnology, TP248.13-248.65
Abstract

We have studied the glucose and glutamine deprivation effect on the expression of nuclear genes encoding mitochondrial proteins in U87 glioma cells in relation to inhibition of inositol requiring enzyme-1 (IRE1). It was shown that glutamine deprivation down-regulated the expression of mitochondrial (NADP+)-dependent isocitrate dehydrogenase 2 (IDH2), malic enzyme 2 (ME2), mitochondrial aspartate aminotransferase (GOT2), and subunit B of succinate dehydrogenase (SDHB) genes in control glioma cells in gene specific manner. At the same time, the expression level of malate dehydrogenase 2 (MDH2) and subunit D of succinate dehydrogenase (SDHD) genes in these cells was not changed upon glutamine deprivation. It was also shown that inhibition of ІRE1 signaling enzyme function in U87 glioma cells modified the glutamine deprivation effect on the expression of all studied genes. Furthermore, the expression of the majority of studied genes was resistant to glucose deprivation, except IDH2 and SDHB genes, which expression levels were slightly down-regulated. Inhibition of IRE1 modified the effect of glucose deprivation on ME2, SDHB, SDHD, and GOT2 genes expression. Therefore, glucose and glutamine deprivation affected the expression level of the majority of nuclear genes encoding mitochondrial proteins in relation to the functional activity of IRE1 enzyme, which is a central mediator of endoplasmic reticulum stress and controls cell proliferation and tumor growth.

Published
2016
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4. ERN1 knockdown modifies the impact of glucose and glutamine deprivations on the expression of EDN1 and its receptors in glioma cells

Author

Yuliia V. Yefimova, Liudmyla O Levadna, Olena O. Khita, Yuliia M. Viletska, Dmytro O. Minchenko, Dariia O. Tsymbal, Dariia A Krasnytska, Oleksandr H. Minchenko, and Myroslava Y. Sliusar

Subjects
0301 basic medicine, Endothelin converting enzyme 1, Endocrinology, Diabetes and Metabolism, Glutamine, Gene Expression, Endothelin-Converting Enzymes, Protein Serine-Threonine Kinases, Diseases of the endocrine glands. Clinical endocrinology, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, ece1, Glioma, Cell Line, Tumor, Gene expression, Endoribonucleases, medicine, Humans, ednra, RNA, Messenger, ednrb, education, Receptor, Gene knockdown, education.field_of_study, Endothelin-1, Chemistry, u87 glioma cells, ern1 knockdown, edn1, medicine.disease, Receptor, Endothelin A, RC648-665, Receptor, Endothelin B, Cell biology, ERN1, 030104 developmental biology, Glucose, 030220 oncology & carcinogenesis, Gene Knockdown Techniques, mrna expression, Signal transduction, glucose and glutamine deprivations
Abstract

Objective. The aim of the present investigation was to study the impact of glucose and gluta-mine deprivations on the expression of genes encoding EDN1 (endothelin-1), its cognate receptors (EDNRA and EDNRB), and ECE1 (endothelin converting enzyme 1) in U87 glioma cells in response to knockdown of ERN1 (endoplasmic reticulum to nucleus signaling 1), a major signaling pathway of endoplasmic reticulum stress, for evaluation of their possible implication in the control of glioma growth through ERN1 and nutrient limitations. Methods. The expression level of EDN1, its receptors and converting enzyme 1 in control U87 glioma cells and cells with knockdown of ERN1 treated by glucose or glutamine deprivation by quantitative polymerase chain reaction was studied. Results. We showed that the expression level of EDN1 and ECE1 genes was significantly up-regulated in control U87 glioma cells exposure under glucose deprivation condition in comparison with the glioma cells, growing in regular glucose containing medium. We also observed up-regulation of ECE1 gene expression in U87 glioma cells exposure under glutamine deprivation as well as down-regulation of the expression of EDN1 and EDNRA mRNA, being more significant for EDN1. Furthermore, the knockdown of ERN1 signaling enzyme function significantly modified the response of most studied gene expressions to glucose and glutamine deprivation conditions. Thus, the ERN1 knockdown led to a strong suppression of EDN1 gene expression under glucose deprivation, but did not change the effect of glutamine deprivation on its expression. At the same time, the knockdown of ERN1 signaling introduced the sensitivity of EDNRB gene to both glucose and glutamine deprivations as well as completely removed the impact of glucose deprivation on the expression of ECE1 gene. Conclusions. The results of this study demonstrated that the expression of endothelin-1, its receptors, and ECE1 genes is preferentially sensitive to glucose and glutamine deprivations in gene specific manner and that knockdown of ERN1 significantly modified the expression of EDN1, EDNRB, and ECE1 genes in U87 glioma cells. It is possible that the observed changes in the expression of studied genes under nutrient deprivation may contribute to the suppressive effect of ERN1 knockdown on glioma cell proliferation and invasiveness.

Published
2021

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