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
AUTHORS (11)
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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