Abstract
ERN1 dependent regulation of TMED10, MYL9, SPOCK1, CUL4A and CUL4B genes expression at glucose and glutamine deprivations in U87 glioma cells
Highlights
M alignant gliomas are highly aggressive tumors and characterized by extensive tumor cell invasion into the normal brain parenchyma
To determine if glucose and glutamine deprivations affect the expression level of genes encoding TMED10, SPOCK1, myosin light chain 9 (MYL9), CUL4A and CUL4B, which play multifunctional role in tumorigenesis, through the ERN1 branch of endoplasmic reticulum stress response, we investigated the effect of glucose and glutamine deprivations on the expression level of these genes in control glioma cells and cells without both enzymatic activities of this signaling protein
To investigate a possible role of endoplasmic reticulum stress signaling mediated by ERN1 enzyme in regulation of the expression of MYL9 gene by glucose deprivation, we investigated the effect of glucose deprivation condition on this gene expression in glioma cells without enzy
Summary
M alignant gliomas are highly aggressive tumors and characterized by extensive tumor cell invasion into the normal brain parenchyma. Cullins (CUL4A and CUL4B) are the core component of multiple cullin-RING-based E3 ubiquitinprotein ligase complexes which mediate the ubiquitination and subsequent proteasomal degradation of target proteins and involved in tumorigenesis [27,28,29,30,31] These cullins play a role in PCNA-dependent polyubiquitination of CDT1 and MDM2-dependent ubiquitination of TP53 as well as in the mammalian target-of-rapamycin (mTOR) pathway involved in control of cell growth, size and metabolism. It is possible that this anti-proliferative effect is mediated by altered expression of TMED10, MYL9, SPOCK1, CUL4A, and CUL4B genes, which are integrated into the unfolded protein response signaling pathways and regulate cell proliferation. The main goal of this study was investigation the effect of glucose and glutamine deprivations on the expression of cancer related genes (TMED10, MYL9, SPOCK1, CUL4A, and CUL4B) in glioma U87 cells in relation to inhibition of ERN1 signaling for evaluation of their possible significance in ERN1 signaling mediated control of glioma cell proliferation
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