ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
Silencing of GLS and overexpression of GLS2 genes cooperate in decreasing the proliferation and viability of glioblastoma cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 56 citations in OpenAlex.
- Targeting Glutaminase Isoforms GLS and GLS2 in Luminal Breast Cancer.International journal of molecular sciences · 2026Article
- Disrupted glutamate homeostasis as a target for glioma therapy.Pharmacological reports : PR · 2024Review
- Cuproptosis in cancer: biological implications and therapeutic opportunities.Cellular & molecular biology letters · 2024Review
- Exploiting the Achilles' heel of cancer: disrupting glutamine metabolism for effective cancer treatment.Frontiers in pharmacology · 2024Review
- The Involvement of Long Non-Coding RNAs in Glutamine-Metabolic Reprogramming and Therapeutic Resistance in Cancer.International journal of molecular sciences · 2022Review
- Targeting Glutaminase by Natural Compounds: Structure-Based Virtual Screening and Molecular Dynamics Simulation Approach to Suppress Cancer Progression.Molecules (Basel, Switzerland) · 2022Article
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- The cuproptosis-related signature associated with the tumor environment and prognosis of patients with glioma.Frontiers in immunology · 2022Article
- TMEM180 contributes to SW480 human colorectal cancer cell proliferation through intra-cellular metabolic pathways.Translational oncology · 2021Article
- The Big Picture of Glioblastoma Malignancy: A Meta-Analysis of Glioblastoma Proteomics to Identify Altered Biological Pathways.ACS omega · 2021Article
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- Aberrant Metabolism as Inductor of Epigenetic Changes in Breast Cancer: Therapeutic Opportunities.Frontiers in oncology · 2021Review
- The Role of Pi, Glutamine and the Essential Amino Acids in Modulating the Metabolism in Diabetes and Cancer.Journal of diabetes and metabolic disorders · 2020Review
- The Regulation of Ferroptosis by Tumor Suppressor p53 and its Pathway.International journal of molecular sciences · 2020Review
- Combined blockade of EGFR and glutamine metabolism in preclinical models of colorectal cancer.Translational oncology · 2020Article
- Targeting Glutamine Addiction in Gliomas.Cancers · 2020Review
- The Epithelial to Mesenchymal Transition Promotes Glutamine Independence by SuppressingCancers · 2019Article
- Article
- Metformin and temozolomide, a synergic option to overcome resistance in glioblastoma multiforme models.Oncotarget · 2017Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamine (Gln) metabolism, initiated by its degradation by glutaminases (GA), is elevated in neoplastic cells and tissues. In malignant glia-derived tumors, GA isoforms, KGA and GAC, coded by the GLS gene, are overexpressed, whereas the GLS2-coded GAB and LGA isoforms, are hardly detectable in there. Our previous study revealed that transfection of T98G glioblastoma cells with GAB reduced cell proliferation and migration, by a yet unknown mechanism not related to Gln degradation. The question arose how simultaneous overexpression of GAB and inhibition of KGA would affect glioblastoma cell growth. Here, we used siRNA to silence the expression of Gls in T98G cells which were or were not stably transfected with GAB (TGAB cells). In both T98G and TGAB cell lines, silencing of Gls with siRNAs targeted at different sequences decreased cell viability and proliferation in a different, sequence-dependent degree, and the observed decreases were in either cell line highly correlated with increase of intracellular Gln (r > 0.9), a parameter manifesting decreased Gln degradation. The results show that combination of negative modulation of GA isoforms arising from GLS gene with the introduction of the GLS2 gene product, GAB, may in the future provide a useful means to curb glioblastoma growth in situ. At the same time, the results underscore the critical role of Gln degradation mediated by KGA in the manifestations of aggressive glial tumor phenotype.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.