Inhibition of tumor immune evasion has also been explored using glycolytic enzyme inhibitors, including 2-deoxy-D-glucose and oxalate. Despite these advances, lactylation-targeted research remains in its early stages and faces notable limitations that warrant further investigation. This review provides insights into the role of lactylation in diverse diseases and highlights emerging therapeutic strategies aimed at modulating lactylation-associated molecular targets.

These findings identify H3K18la-mediated FOXM1 activation as a novel mechanism underlying DTX resistance in PCa. Ica-Cur may represent a promising therapeutic agent by targeting lactylation-dependent epigenetic regulation and FOXM1-driven transcriptional activity, supporting its clinical potential for overcoming chemoresistance.

QJZG effectively improved renal injury in SLE by reducing inflammation and modulating the AMPK/ULK1 signalling pathway to suppress M1 macrophage polarisation.

Background/Objectives: Melanoma cells enhance glycolysis and expand lysosomes to support energy metabolism, proliferation, and metastasis. However, mefloquine and siramesine induced stronger LMP in A375 cells than in fibroblasts and showed melanoma-selective toxicity when combined with 2DG. 2DG-mediated glycolysis inhibition in combination with lysosomal destabilization induced by mefloquine and siramesine, but not with non-selectively toxic LLOMe, may be promising antimelanoma strategy.

The impact of glycolytic inhibition by 2-Deoxy-D-glucose (2-DG) on CAR-NK92 antitumor capacity was examined...Conclusion ATPIF1 regulates the antitumor activity of CAR-NK92 cells through modulating glycolytic metabolism. Overexpression of ATPIF1 can enhance the antitumor efficacy of CAR-NK92 cells.

This was achieved using 2-deoxy-D-glucose (2DG) alone, 2DG combined with metformin, or Poly(2-hydroxyethyl methacrylate) (polyHEMA)-coated surfaces. These clones also demonstrated enhanced detachment properties and upregulation of proto-oncogenes, in addition to their senescent-like phenotype. Critically, the uncoupling of CD274 transcription from surface PD-L1 expression suggests a potential therapeutic vulnerability that could be exploited in TNBC.

Based on these findings, we show that pharmacologic glycolysis inhibition with 2-deoxyglucose (2-DG) reverses immune resistance in GSNOR-KO models, enhancing CD8+ T-cell infiltration and sensitizing tumors to anti-PD-1 therapy both in vitro and in vivo. Notably, this is the first demonstration that metabolic intervention can restore immune sensitivity in GSNOR-deficient CRC. Our results identify GSNOR expression as a predictive biomarker for metabolic-immune combinatorial strategies and support the clinical translation of 2-DG plus anti-PD-1 as a precision immunotherapy approach for this high-risk CRC phenotype.

Notably, 2-DG also inhibited EBV lytic reactivation in AGS-EBV cells under hypoxic conditions. These findings provide valuable insights into the molecular mechanisms of EBV-mediated metabolic reprogramming and highlight the potential of 2-DG as a therapeutic agent for EBVaGC.

Our study revealed, for the first time, that BA ameliorated liver fibrosis by directly targeting CEBPZ, disrupting its LLPS, and activating the p53/HK2 axis to induce HSC senescence. This work uncovered a novel plant-derived therapeutic strategy targeting a previously unrecognized CEBPZ-LLPS/p53/HK2 mechanism in hepatic fibrosis.

Herein, we developed a mito-specific "Trojan Horse" nanoplatform (2-pN@LNPs) coloaded with Niclosamide (Nic) and 2-deoxy-d-glucose (2-DG) to attack key metabolism pathways and synergistically ignite pyroptosis for restoring antitumor immunity. Moreover, the synergistic treatment regimen can promote cytotoxic and helper T cells (CD8+/CD4+ T cells) recruitment and M1-type macrophage polarization, facilitating the establishment of a boost in immunological memory to prevent recurrence and metastasis. Overall, this work provides a robust strategy targeting metabolism through mitochondrial uncoupling and glycolysis inhibition, which can effectively improve the antitumor effect, inhibit lung metastasis, and help modulate antitumor immunity.

Expression of myogenesis and inflammation markers, GLUT4 translocation, [3H]2-deoxyglucose uptake, and intramyocellular insulin signalling were determined...Moreover, breast cancer CM inhibits basal and insulin-mediated GLUT4 translocation and glucose uptake, likely by blocking insulin-stimulated Rac1, but not Akt-TBC1D4 activation. These results underscore a potential mechanistic link between breast cancer and metabolic disorders and suggest that skeletal muscle rewiring may play a role.

TU686 cells were treated with TAMEMsC-h derived Exos, cisplatin (DDP), 2-deoxyglucose, and small-interfering-GLUT-1, with TAMEMsC-h morphology and phenotype assessed. TAM-Exos boosted aerobic glycolysis by mediating WTAP/GLUT-1, thus decreasing DDP sensitivity and enhancing tumour growth. TAM-Exos promoted the m6A modification of GLUT-1 through WTAP, and improved GLUT-1 mRNA stability and expression, thereby promoting aerobic glycolysis and reducing the chemo-sensitivity of LC.