PFKL (Phosphofructokinase, Liver Type)

Moreover, DT-13 improved the anticancer effects of sorafenib in HCC. In summary, this study provided evidence for the potential application of DT-13 in HCC treatment.

For left-sided colon cancer, glucose-6-phosphate (G6P), ATP, ADP, glycerol, and palmitoyl-CoA were key metabolites forming the basis of the gene-metabolite network, along with genes including G6PD, PFKL, MAPK14, FLT1, CDK4, AURKA, MAP2K1, ERCC3, TP53, WEE1, and GPD2. These findings highlight distinct molecular profiles between right- and left-sided colon cancers, particularly in pathways related to angiogenesis, apoptosis, ferroptosis, and fatty acid metabolism, which may inform therapeutic strategies.

The electrophile-drug conjugate (EDC) site-specifically and proteome-wide selectively modifies K677 in the allosteric effector site to stabilize the R-state tetramer of PFKL and destabilize cell metabolism. We introduce EDCs as a new delivery mechanism analogous to antibody-drug conjugates but differentiated by selective covalent targeting of intracellular proteins.

In vivo, HIF-1α knockdown inhibited tumor growth and CD8⁺T cell infiltration, while PFKL restoration reversed these phenotypes. Our study unveils HIF-1α-driven m6A modification as a critical link between MDSC metabolism and CSC immune evasion, proposing the HIF-1α/YTHDF2/PFKL axis as a therapeutic target for HCC.

These findings indicate that both catalytic activity and subcellular localization are required for directional migration in breast cancer cells. These results suggest a novel function of PFKL filaments in cells and provide insight into the function of compartmentalized glycolysis in the cytoplasm.

Based on the mechanism of PFKL facilitates the efficacy of romidepsin, we developed a therapeutic peptide, PFKL-552-572-R8, which significantly enhances the antitumor effect of romidepsin both in vitro and in vivo. Our findings reveal that spatiotemporal regulation confers a moonlight function to PFKL as an endogenous HDAC inhibitor to maintain the stability of epigenetic modifications and highlight PFKL as a promising therapeutic target for enhancing the clinical utility of HDACi in solid tumors.

In summary, our study revealed that piR-35410 promotes the malignant progression of TNBC by regulating PFKL-mediated glycolysis. These findings provide valuable insights into the role of piR-35410 in TNBC pathogenesis, revealing its potential as a novel 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.

This study demonstrated the inhibitory effects of esculetin against liver cancer both in vitro and in vivo, demonstrating inhibition of glycolysis in liver cancer cells. In addition, the key glycolysis enzyme GPI was identified as a direct target of esculetin.

The study identified 7 key TMRGs with significant prognostic value in BC. The constructed model effectively stratifies patient risk, providing a foundation for targeted therapies and personalized treatment strategies.

Moreover, the administration of alpha-lipoic acid (ALA) leads to a reduction in KLF7 expression in cells and tumor tissues, a suppression of the proliferation, migration, and invasion of HeLa and SiHa cells ( P<0.05), and an increase in the carcinogenic potential of HeLa cells ( P<0.05), while KLF7 overexpression shows the opposite effect on the expressions of ACADL and PFKL in HeLa and SiHa cells. In conclusion, KLF7 promotes the development of cervical cancer, and ALA can downregulate KLF7 expression and play a positive role in cervical cancer treatment.

These findings suggest that sLZIP contributes to the metabolic reprogramming of prostate cancer cells via the transcriptional regulation of PGK1.