Abstract:
:Given the known anti-tumorigenic properties of IFNγ, its effect on glioma cell survival was investigated. Though IFNγ had no effect on glioma cell viability, it induced cell cycle arrest. This was accompanied by increased expression of p53 and retinoic acid inducible gene (RIG-I). While RIG-I had no effect on glioma cell survival, it increased expression of p53 and its downstream target TP53 induced glycolysis and apoptosis regulator (TIGAR). IFNγ induced mitochondrial co-localization of RIG-I was concomitant with its ability to regulate ROS generation, oxidative phosphorylation (OXPHOS) and key enzymes involved in glycolysis and pentose phosphate pathway. Importantly, metabolic gene profiling indicated a suppressed glycolytic pathway in glioma cells upon IFNγ treatment. In addition, IFNγ mediated increase in casein kinase 2 (CK2) expression positively regulated RIG-I expression. These findings demonstrate how IFNγ induced CK2 regulates RIG-I to drive a complex program of metabolic adaptation and redox homeostasis, crucial for determining glioma cell fate.
journal_name
Cytokinejournal_title
Cytokineauthors
Ghildiyal R,Sen Edoi
10.1016/j.cyto.2015.10.009subject
Has Abstractpub_date
2017-01-01 00:00:00pages
219-228eissn
1043-4666issn
1096-0023pii
S1043-4666(15)30080-6journal_volume
89pub_type
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