2-Deoxy-D-glucose (2DG), a glycolytic inhibitor, depleted ATP dose-dependently (30-300 μM) and prevented those increases both at the protein and transcriptional levels. This was also observed in 3D spheroids upon TGF-β transient siRNA-mediated silencing or when TGF-βR1 kinase activity was inhibited by galunisertib...3D spheroids require ATP and a TGF-β/TGF-βR1 autocrine signaling axis to recapitulate the apoptosis/autophagy phenotypes. Combining glycolysis inhibition with TGF-β signaling inhibition could offer a promising therapeutic strategy for this rare and lethal brain cancer.

Functionally, TBK1 promoted cell proliferation and colony formation while inhibiting apoptosis, which were attenuated by the glycolytic inhibitor 2-deoxy-D-glucose. These findings establish TBK1 as a critical mediator linking GM dysbiosis to metabolic reprogramming in CRC, suggesting that targeting the TBK1-glycolysis axis may represent a promising therapeutic strategy for delaying CRC progression.

Pristimerin effectively ameliorates gastric mucosal pathological damage and oxyntic atrophy in high-dose tamoxifen-induced SPEM mice, and improves SPEM progression by modulating Cdkn1c (p57)-mediated glycolytic reprogramming.

Mechanistically, SpD increased tumor suppressor VHL expression level, down-regulated expression level of electron transport chain enzymes, generated reactive oxygen species, induced mitochondrial dysfunction, and triggered Bax/Bak-mediated apoptosis. These findings highlighted the synergistic anticancer potential of SpD in combination with 2-DG in aggressive breast cancer, offering insights into improved clinical outcomes in the future.

Our findings indicate that CRIP1 knockdown induces a glycolytic switch in AML cells, rendering them exquisitely sensitive to glycolytic inhibition by 2-DG. This suggests that CRIP1 status could serve as a biomarker for predicting response to metabolic therapies and highlights 2-DG as a promising therapeutic agent for a subset of AML characterized by glycolytic dependency.

This study revealed a novel mechanism in which BMAL1 downregulation under aging and HFD conditions promotes NASH progression by binding to HIF-1α and modulating the glycolysis-NLRP3 inflammasome axis.

Importantly, the pharmacologic inhibition of glycolysis with 2-deoxy-d-glucose restored SOCS3 secretion in these AMs. Together, our findings demonstrate that lung tumor-associated AMs undergo a time-dependent metabolic shift toward glycolysis, resulting in impaired SOCS3 secretion-a phenotype that can be reversed by targeting glycolytic flux. These results highlight a potential therapeutic approach for modulating immune suppression in the tumor microenvironment.

Advanced multimetabolic APTw-CEST and 2-deoxy-D-glucose-CEST postprocessing metrics allowed adequate preclinical murine BC subtyping. AREX showed potential for 2-deoxy-D-glucose-CEST in tumor characterization; however, APTw-CEST remains superior. MTRasym failed to distinguish between tumor subtypes in CEST-MRI.

In vivo, NAT10 promoted tumor growth. Collectively, NAT10 contributes to RB progression by enhancing glycolysis through ac4C-mediated PFKFB3 mRNA stabilization, identifying the NAT10-ac4C-PFKFB3 axis as a potential therapeutic target.

Lactylation at K873 stabilized HK2 by inhibiting its ubiquitination, which in turn drove glycolytic flux and promoted malignant behaviors in DDP-resistant NSCLC. This HK2 lactylation-stabilization axis represents a novel mechanism underlying chemoresistance and a promising therapeutic target for overcoming DDP resistance in NSCLC.