PFKP (Phosphofructokinase, Platelet)

In vitro, XAV939 suppressed β-catenin-driven aerobic glycolysis in TNBC cells, downregulating β-catenin and glycolytic proteins, reducing glycolytic activity, and impairing aggressive phenotypes (proliferation, migration, invasion, clonogenicity).ConclusionOverall, our results highlight the crucial role of β-catenin in controlling aerobic glycolysis via regulation of key glycolytic proteins, thereby positively driving the progression and metastasis of TNBCs. Additionally, our data strongly establish that XAV939 effectively inhibits glycolytic phenotype, thereby suggesting its therapeutic potential in TNBC patients.

CAF exposure enhanced SIAH2 expression, CSC spheroid growth, and resistance to fluorouracil, leucovorin, and oxaliplatin (FOLFOX) chemotherapy, whereas SIAH2 depletion effectively abrogated these effects. Collectively, these findings identify the SIAH2/WNK1 axis as a central metabolic regulator linking glycolysis, CSC maintenance, and microenvironment-driven therapy resistance in CRC, highlighting its potential as a therapeutic target.

Moreover, we demonstrated that Suramin effectively suppressed CC tumor growth by inhibiting PFKP-mediated glycolysis. Our findings provide a robust prognostic model and disclose PFKP as a potential therapeutic target in CC, offering insightful guidance on cancer management of CC patients.

Besides, according to in vivo studies, the combination of RSL3 and Dox further suppressed BC tumor growth without inducing significant adverse effects. On these accounts, RSL3 makes BC cells more sensitive to Dox by inducing glycolytic dysfunction, implying that RSL3/Dox co-treatment could be a viable therapeutic approach for BC patients.

This study illuminates PBRM1's tumor suppressor role, highlighting the AKT-mTOR pathway and aerobic glycolysis as potential therapeutic targets in NPC.

Finally, treatment with losartan pharmacologically inhibits the ISGylation of DPP3, preventing its secretion via sEVs. In summary, our findings demonstrate that DPP3, which is encapsulated in sEVs and secreted by breast cancer cells, regulates angiogenesis in the lung and remodels vascular niches to promote breast cancer lung metastasis, making it a potential target for the diagnosis and treatment of breast cancer metastasis.

Furthermore, overexpression of CAB39L partially counteracted the promoting effects of high levels of miR-3662 on the malignant biological phenotype of GC cells. In conclusion, this study reveals that miR-3662 acts as a carcinogenic regulator in GC by targeting CAB39L, with the underlying mechanism potentially involving the modulation of AMPK activation to enhance cellular glycolysis.

Functional assays demonstrated that silencing C1QBP or PFKP increased intracellular copper concentration, suppressed proliferation, and inhibited invasion, mechanistically linking these genes to cuproptosis dysregulation. Our findings nominate C1QBP/PFKP as actionable targets for LUAD therapy, offering both prognostic biomarkers and copper-metabolism-directed treatment strategies.

The retraction has been agreed to because the evidence of image re-use and manipulation both with a previous article and within the same article fundamentally compromises the editors' confidence in the results presented. The authors did not respond to the notice regarding the retraction.

The identified genes-KIF2C, MKI67, HMGA1, PFKP, and CCNA2-are highly expressed in cancerous tissues and correlate with LUAD prognosis. These findings highlight their value as tumor biomarkers and therapeutic targets, offering new opportunities for targeted LUAD treatments.

These findings highlight a potential therapeutic vulnerability in LUSC metabolic regulation. [Image: see text] The online version contains supplementary material available at 10.1186/s40364-025-00815-w.

Our study characterizes the metabolic heterogeneity of CRC and suggests a potential role for HGS cells in shaping the tumor microenvironment. The molecular features identified here may offer insights into metabolic dependencies that could be explored for future therapeutic targeting.