Inhibition of ERN1 affects the expression of TGIF1 and other homeobox gene expressions in U87MG glioblastoma cells

Minchenko, Oleksandr H.; Khita, Olena O.; Krasnytska, Daria A.; Viletska, Yuliia M.; Rudnytska, Olha V.; Hnatiuk, Oksana S.; Minchenko, Dmytro O.

doi:10.1016/j.abb.2024.110073

Archives of Biochemistry and Biophysics

2024

DOI: 10.1016/j.abb.2024.110073

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Inhibition of ERN1 affects the expression of TGIF1 and other homeobox gene expressions in U87MG glioblastoma cells

Oleksandr H. Minchenko,

Olena O. Khita,

Daria A. Krasnytska

et al.

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2024

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Cited by 3 publications

References 40 publications

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Knockdown of ERN1 disturbs the expression of phosphoserine aminotransferase 1 and related genes in glioblastoma cells

Minchenko,

Sliusar,

Khikhlo

et al. 2024

Archives of Biochemistry and Biophysics

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Knockdown of ERN1 disturbs the expression of phosphoserine aminotransferase 1 and related genes in glioblastoma cells

Minchenko,

Sliusar,

Khikhlo

et al. 2024

Archives of Biochemistry and Biophysics

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Endoplasmic reticulum stress-dependent regulation of carboxypeptidase E expression in glioblastoma cells

Minchenko,

Abramchuk,

Khita

et al. 2024

Endocrine Regulations

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Objective. Carboxypeptidase E (CPE) plays an important role in the biosynthesis of neurotransmitters and peptide hormones including insulin. It also promotes cell proliferation, survival, and invasion of tumor cells. The endoplasmic reticulum stress, hypoxia, and nutrient supply are significant factors of malignant tumor growth including glioblastoma. There are data indicating that the knockdown of the endoplasmic reticulum to nucleus signaling 1 (ERN1) suppressed glioblastoma cell proliferation and increased invasiveness of these cells. The present study aims to investigate the regulation of the CPE gene in U87MG glioblastoma cells by ERN1 knockdown, hypoxia, and glucose or glutamine deprivations with the intent to reveal the role of ERN1 signaling in the regulation of this gene expression and function in tumorigenesis. Methods. Human glioblastoma cells U87MG (transfected by an empty vector; control) and ERN1 knockdown cells with inhibited ERN1 endoribonuclease and protein kinase (dnERN1) or only ERN1 endoribonuclease (dnrERN1) were used. Hypoxia was introduced by dimethyloxalylglycine; for glucose and glutamine deprivations, the cells were cultured in DMEM medium without glucose or glutamine for 16 h, respectively. The expression level of the CPE gene was studied by quantitative RT-PCR and normalized to ACTB. Results. It was found that inhibition of endoribonuclease and protein kinase activities of ERN1 led to a strong up-regulation of CPE gene expression in glioblastoma cells. The expression of this gene also increased in glioblastoma cells after silencing ERN1. At the same time, the expression of this gene did not significantly change in cells with inhibited ERN1 endoribonuclease only. The expression of the CPE gene was resistant to hypoxia in control U87MG cells, but increased in cells with ERN1 knockdown. The expression of this gene was up-regulated under glutamine deprivation in control glioblastoma cells, but decreased upon ERN1 knockdown. However, glucose deprivation decreased the expression of CPE gene in both types of used cells, but ERN1 inhibition enhanced this effect. Conclusion. The results of the present study demonstrate that inhibition of ERN1 strongly up-regulated the expression of pro-oncogenic CPE gene through protein kinase activity of ERN1 and that increased CPE gene expression possibly participates in ERN1 knockdown-mediated invasiveness of glioblastoma cells.

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The expression of DNAJB9 in normal human astrocytes is more sensitive to nanographene oxide than in glioblastoma cells

Minchenko,

Kulish,

Viletska

et al. 2024

Endocrine Regulations

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Objective. Nanographene oxide (nGO) nanoparticles (NPs) have unique properties and are widely used in various fields, including biomedicine. These NPs, however, also exhibit toxic effects and therefore, the understanding of the molecular mechanism of nGO toxicity is very important mainly for the nanomedicine, especially the cancer therapy. This study aimed to examine the impact of nGO NPs on the expression of genes associated with endoplasmic reticulum (ER) stress, proliferation, and cancerogenesis in both normal human astrocytes and U87MG glioblastoma cells. Methods. Normal human astrocytes line NHA/TS and U87MG glioblastoma cells stable transfected by empty vector or dnERN1 (dominant-negative construct of ERN1) were exposed to low doses of nGO (1 and 4 ng/ml) for 24 h. RNA was extracted from the cells and used for cDNA synthesis. The expression levels of DNAJB9, EDEM1, DDIT3, ATF3, ATF4, TOB1, and IDH2 mRNAs were measured by quantitative polymerase chain reaction and normalized to ACTB mRNA. Results. We showed that treatment of normal astrocytes and glioblastoma cells by relatively small doses of nGO (1 and 4 ng/ml for 24 h) affected the expression level of DNAJB9, EDEM1, DDIT3, ATF3, ATF4, TOB1, and IDH2 mRNAs, but the sensitivity of all studied mRNA expressions to these NPs was significantly higher in normal astrocytes than in glioblastoma cells. The impact of nGO on these gene expressions is mediated by ER stress because ERN1 knockdown suppresses the effect of these nanoparticles in glioblastoma cells. Conclusion. The data obtained demonstrate that the low doses of nGO disturbed the functional integrity of the genome preferentially through ER stress signaling and exhibit a more pronounced genotoxic effect in the normal astrocytes than the glioblastoma cells.

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Inhibition of ERN1 affects the expression of TGIF1 and other homeobox gene expressions in U87MG glioblastoma cells

Cited by 3 publications

References 40 publications

Knockdown of ERN1 disturbs the expression of phosphoserine aminotransferase 1 and related genes in glioblastoma cells

Knockdown of ERN1 disturbs the expression of phosphoserine aminotransferase 1 and related genes in glioblastoma cells

Endoplasmic reticulum stress-dependent regulation of carboxypeptidase E expression in glioblastoma cells

The expression of DNAJB9 in normal human astrocytes is more sensitive to nanographene oxide than in glioblastoma cells

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