The NF-κB member p65 controls glutamine metabolism through miR-23a

Rathore, Moeez Ghani; Saumet, Anne; Rossi, Jean François; Bettignies, Carine de; Tempé, Denis; Lecellier, Charles-Henri; Villalba, Martín

doi:10.1016/j.biocel.2012.05.011

Cited by 111 publications

(103 citation statements)

References 40 publications

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“…The GLS transcript has a pH-responsive element, which results in increased expression at acidic pH [104][105][106]. The transcription factor c-Myc indirectly upregulates GLS in some contexts by repressing the expression of miRNA-23 [96,107], which is also repressed by NF-κB [108]. The transcription factor c-Jun can directly bind to the GLS gene promoter and enhance expression, and other recent reports have shown that the transcriptional coactivator PGC-1α, and loss of the tumor suppressor Rb, increase GLS transcription and translation, respectively [109][110][111].…”

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confidence: 99%

A Tale of Two Glutaminases: Homologous Enzymes with Distinct Roles in Tumorigenesis

2017

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Many cancer cells exhibit an altered metabolic phenotype, in which glutamine consumption is upregulated relative to healthy cells. This metabolic reprogramming often depends upon mitochondrial glutaminase activity, which converts glutamine to glutamate, a key precursor for biosynthetic and bioenergetic processes. Two isozymes of glutaminase exist, a kidney-type (GLS) and a liver-type enzyme (GLS2 or LGA). While a majority of studies have focused on GLS, here we summarize key findings on both glutaminases, describing their structure and function, their roles in cancer and pharmacological approaches to inhibiting their activities.

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confidence: 99%

A Tale of Two Glutaminases: Homologous Enzymes with Distinct Roles in Tumorigenesis

2017

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“…c-Myc promoted GLS expression by suppressing GLS repressor miR-23a/b in human P-493 B-lymphoma cells and human leukemic Jurkat cells. 23,24 miRNA-153 displayed low levels in GBM tissues and cell lines. It is possible that c-Myc may promote GLS expression in GBM by negatively regulating the GLS-targeting miRNA-153 in GBM, which further enhances the utilization of glutamine.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-153 regulates glutamine metabolism in glioblastoma through targeting glutaminase

Liu

Wang

et al. 2017

Tumour Biol.

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Glioblastoma is the most aggressive manifestation of malignant gliomas and considered to be among the deadliest forms of human cancers. MicroRNAs are found to tightly regulate diverse biological processes and considered to play important roles in cancer etiology. In this study, we found that microRNA-153 was significantly downregulated in glioblastoma tissues compared to matched non-tumor tissues and in glioblastoma cell lines. To investigate the potential function of microRNA-153 in glioblastoma, we transfected glioblastoma cell line U87MG as well as U373MG with synthetic microRNA-153 oligos and observed decreased cell proliferation and increased apoptosis. We further found that microRNA-153 restrained glutamine utilization and glutamate generation. Bioinformatics analysis revealed that glutaminase, which catalyzed the formation of glutamate from glutamine, is the potential target of microRNA-153. Indeed, microRNA-153 cannot further reduce glutamine utilization when glutaminase was knocked down. Overexpression of glutaminase abrogates the effect of microRNA-153 on glutamine utilization. Furthermore, the relative expression of microRNA-153 and glutaminase in glioblastoma versus matched non-tumor tissues showed a reverse correlation, further indicating that microRNA-153 may negatively regulate glutaminase in vivo. These results demonstrate an unexpected role of microRNA-153 in regulating glutamine metabolism and strengthen the role of microRNA-153 as a therapeutic target in glioblastoma.

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“…A literature survey shows that metastasis and growth of brain tumor is inhibited by targeting glutamine metabolism (38) and increased expression of Notch1 (39), respectively. Again, Jurkat, a T-cell acute lymphoblastic leukemia cell line that harbors activated Notch1 pathway, has a lower growth rate in high glutamine media, which increases upon inducing glutamine utilization ability (29). The process of naïve T-cell activation is a highly glutamine-dependent process (40) and is inhibited by the activation of Notch pathway (41).…”

Section: Discussionmentioning

confidence: 99%

“…This cell line has been reported earlier to have an impaired glutamine utilization capability (29) and has been used for studying change in glutamine dependence for various functions (30). Hence, first the exogenous glutamine dependence of Jurkat cells for cell survival and ADP/ATP ratio maintenance was studied.…”

Section: Alteration Of the Expression Of Proteins Involved In Glutamimentioning

confidence: 99%

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Alteration of Mitochondrial Proteome Due to Activation of Notch1 Signaling Pathway

Basak

Roy²,

Banerjee

2014

Journal of Biological Chemistry

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The NF-κB member p65 controls glutamine metabolism through miR-23a

Cited by 111 publications

References 40 publications

A Tale of Two Glutaminases: Homologous Enzymes with Distinct Roles in Tumorigenesis

A Tale of Two Glutaminases: Homologous Enzymes with Distinct Roles in Tumorigenesis

MicroRNA-153 regulates glutamine metabolism in glioblastoma through targeting glutaminase

Alteration of Mitochondrial Proteome Due to Activation of Notch1 Signaling Pathway

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