Expression of IDE and PITRM1 genes in ERN1 knockdown U87 glioma cells: effect of hypoxia and glucose deprivation

microrna Protein Serine-Threonine Kinases Insulysin Diseases of the endocrine glands. Clinical endocrinology pitrm1 03 medical and health sciences Cell Line, Tumor Endoribonucleases Humans 0303 health sciences ide hypoxia u87 glioma cells Brain Neoplasms glucose deprivation ern1 knockdown Metalloendopeptidases Glioma RC648-665 Endoplasmic Reticulum Stress Cell Hypoxia 3. Good health Gene Expression Regulation, Neoplastic Glucose Gene Knockdown Techniques mrna expression Signal Transduction
DOI: 10.2478/enr-2020-0021 Publication Date: 2020-08-28T14:46:14Z
ABSTRACT
Abstract Objective. The aim of the present investigation was to study expression genes encoding polyfunctional proteins insulinase (insulin degrading enzyme, IDE) and pitrilysin metallopeptidase 1 (PITRM1) in U87 glioma cells response inhibition endoplasmic reticulum stress signaling mediated by ERN1/IRE1 (endoplasmic nucleus 1) for evaluation their possible significance control metabolism through ERN1 as well hypoxia, glucose glutamine deprivations. Methods. level IDE PITRM1 studied knockdown under deprivations hypoxia quantitative polymerase chain reaction. Results. It found that down-regulated (without protein kinase endoribonuclease activity) comparison with cells, being more significant gene. We also up-regulation microRNA MIR7-2 MIRLET7A2, which have specific binding sites 3’-untranslated region mRNAs, correspondingly, can participate posttranscriptional regulation these mRNA expressions. Only did not change significantly cells. is preferentially regulated kinase. showed enzyme function modified gene expressions hypoxia. Glucose deprivation increased genes, but enhanced only effect on expression. Glutamine affect both types up-regulated this stronger Conclusions. Results demonstrate decreases mechanism. sensitive dependent gene-specific manner. a result complex interaction variable related unrelated regulatory factors contributed cell metabolism.
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