GLS1 (Glutaminase)

Co-expression of these key metabolic enzymes remains a promising candidate as prognostic markers and therapeutic targets. Concurrent targeting of these metabolic pathways may offer novel therapeutic opportunities for patients with advanced-stage gastric cancer.

Through ultrasound-potentiated suppression of GLS1-driven metabolic and AKT signaling pathways, R13, a new oridonin derivative, exhibits strong anti-MM action with little systemic toxicity. These results support the combination of drugs originating from Traditional Chinese Medicine with noninvasive ultrasound techniques to enhance treatment efficacy while preserving safety, and they show R13 as a good option for ultrasound-augmented biotherapy in MM.

This study demonstrates that α-KG preconditioning significantly enhances ADSC survival and therapeutic efficacy in burn wound healing through HIF-1α-mediated metabolic reprogramming. HIF-1α activation coordinately upregulates glutamine-driven GSH synthesis for redox homeostasis and glycogen storage for bioenergetic resilience, providing a dual mechanism of cytoprotection. These findings establish metabolic preconditioning as a potent, translatable strategy to improve the efficacy of stem cell-based therapies not only in wound healing but potentially in other ischemic and inflammatory conditions characterized by poor cell survival.

Overexpression of GLS or c-Myc rescued the CENPF knockdown's inhibitory effect on GC cell growth. Our findings identify a new CENPF/c-Myc/GLS axis that affects glutamine metabolism and cell survival in GC, implying that CENPF might be a novel target for the treatment of GC.

This study demonstrates that combining long-read spatial transcriptomics with patient-derived organoid models provides a powerful and scalable approach for dissecting gene and isoform-level heterogeneity in ccRCC and for elucidating spatially resolved transcriptional responses to novel therapeutics.

Glutamine and glucose consumption, chemosensitivity to cisplatin and paclitaxel, and doubling time were analyzed in three ovarian carcinoma cell lines (ES-2, TOV-21G: clear cell; OVCAR-3: serous papillary) and primary ascites cells under varying glutamine concentrations (0.5, 1, 2, 4 mM). Intense glutaminolysis is associated with increased tumor aggressiveness, suggesting a prognostic role for 18F-(2S,4R)-4-fluoroglutamine (18F-fluoroglutamine) positron emission tomography (PET) imaging. Glutamine supplementation, without impacting chemoresistance, may mitigate iatrogenic effects, while targeting glutaminolysis offers a therapeutic perspective.

Ultimately, these findings suggest that canine OMM does not heavily rely on mGluR1 for tumorigenesis or progression. Differential GLS1 protein expression warrants further investigation with protein quantification.

Critically, this novel metabolic-epigenetic axis requires the catalytic function of GCDH. These findings not only reveal a novel metabolic-epigenetic axis driven by a specific mitochondrial enzyme but also suggest GCDH as a potential therapeutic target in breast cancer.

FOXA2 accelerated BCa cell proliferation and metastasis by promoting GLS1-mediated glutamine metabolism, providing a novel therapy target for BCa.

CB-839 increased the potency of STM2457 only in the LCC9 and ZR-75-1-4-OHT endocrine-resistant cells. Our collective findings suggest that METTL3 inhibition leads to selective glycolytic and oxidative metabolic changes between these endocrine-sensitive and resistant BC cells that can be exploited for combinatorial therapy.

Our study provides initial insights into the oncogenic roles of GLS1 across different tumors. These findings suggest that GLS1 can serve as a potential biomarker for determining prognosis and designing therapeutic strategies for various tumor types.

Inhibiting GLS1 with CB-839 significantly impacted glutamine metabolism in HCC cells while showing limited activity on normal hepatocytes...Overexpressed GLS1 and loss of GLS2 within tumors convey an unfavorable prognosis in patients with HCC. Pharmacological inhibition of GLS1 in HCC cells successfully harnesses glutamine metabolism, representing an attractive target for novel therapeutic approaches.