PFKM (Phosphofructokinase, Muscle)

TSZAF mc inhibits ovarian cancer progression by regulating the AKT/ FOXO3A-mediated glycolysis pathway, which may represent one of the mechanisms underlying the clinical efficacy of TSZAF in ovarian cancer treatment.

Quercetin inhibits glycolysis and tumor progression in a cell line-dependent manner, involving PI3K/AKT signaling predominantly in HOS cells. In summary, our work revealed a substantial quantitative difference between the cellular fractions of OS in which quercetin strongly slowed glycolysis.

The integration of transcriptomic and metabolomic data demonstrated that kisspeptin exerts broad inhibitory effects on metabolism, particularly glucose metabolism, also suggesting potential antitumor effect. Our results suggest kisspeptin as a potential therapeutic target for hepatocellular carcinoma in patients with metabolic syndrome.

Our results provide novel insights into BL pathogenesis, emphasizing the interplay of age and EBV in shaping molecular landscapes. This study underscores the need for multi-omics integration to advance precision therapy strategies for BL subtypes.

Translational studies involving organoid models and xenograft tumor models revealed that the use of FTO inhibitors significantly suppressed PDAC growth. Our findings uncover that targeting the m6A-dependent FTO/C-Jun/PFKM glycolysis regulatory axis may be essential for the prevention and treatment of PDAC.

This study identifies NSUN2 as a critical regulator of TNBC progression through tRNAVal-CAC m5C modification and codon-biased translation of glycolysis-related mRNAs. Our findings reveal a novel NSUN2-tRNAVal-CAC axis that orchestrates metabolic reprogramming and translational control in TNBC, offering a promising prognostic biomarker and therapeutic target.

The isoform-specific modification networks unveil novel targets for developing diagnostic biomarkers and tissue-selective therapeutic strategies. This work not only reestablishes the central role of PFK-1 in tumour metabolic plasticity but also offers a fresh perspective for overcoming cancer treatment challenges.

The NSUN2-mediated GLUT1 stabilization enhances the competitive advantage of tumor cells in glucose acquisition, creating a positive feedback loop that accelerates malignancy and exacerbates CD8+ T cell dysfunction. Building on these insights, we designed a dual-targeting strategy combining GLUT1/NSUN2 axis inhibitor WZB117 with PD-L1 blockade, which synergistically suppressed tumor evolution and reversed immunosuppression in preclinical models, suggesting a novel synergistic therapeutic strategy for treatment-resistant HCC.

We further showed that inhibition of miR-122-5p alleviated the suppression of glycolysis induced by TUG1 depletion. Together, our RNA-seq analysis of TUG1-depleted HCC cells, combined with clinical data, reveals the critical function of TUG1 in promoting glycolysis via sponging miR-122-5p, which is a negative regulator of multiple glycolytic enzymes.

Disrupting citrate-PFKM or PFKM-H3 interactions reduces H3S10 phosphorylation, delays mitosis, and suppresses tumor growth and T-cell proliferation. Our findings demonstrate that PFKM acts as a citrate sensor, coupling metabolic signals to cell cycle regulation.

Overexpression of CNTN1 reversed the inhibitory effects of PFKM knockdown on GC progression. Our research showed that increasing PFKM levels accelerated GC development by regulating CNTN1 expression through mechanisms involving histone lactylation, which could potentially contribute to novel approaches in diagnosing and treating GC.

LRGs play a significant role in endometrial cancer by influencing cell growth, the immune microenvironment, and drug response. The six DLRGs included in the risk model may serve as potential prognostic markers and therapeutic targets for EC.