PKM (Pyruvate Kinase M1/2)

The observed reductions in tumor burden and key biomarkers corroborate the therapeutic potential of this approach. Collectively, these preclinical findings suggest that electroacupuncture and moxibustion, as non-pharmacological adjunctive therapies, hold translational potential for modulating tumor metabolism and slowing HCC progression, warranting further clinical investigation.

In vivo, RHART significantly suppressed tumor growth and expression of CPSF6, MCT4, PCNA, and PKM2, while enhancing cleaved caspase-3. These findings provide scientific evidence that RHART induces apoptotic and metabolic reprogramming effects in hepatocellular carcinoma by targeting the CPSF6/MCT4/c-Myc signaling axis, underscoring its potential as a novel natural therapeutic candidate for liver cancer.

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.

Finally, we propose future research directions regarding the role of lactate in bone diseases. This review highlights lactate as a strategic node that coordinates the bone immune-metabolic network, offering a promising target for the precise regulation of skeletal homeostasis and inflammation.

Therapeutically, combined treatment with the BRD4 inhibitor JQ1 or the first bromodomain (BD1) selective inhibitor MS402 and an anti-GM-CSF antibody markedly suppressed TNBC progression and converted the tumor immune microenvironment from "cold" to "hot". In conclusion, our study reveals a previously unrecognized metabolic-epigenetic mechanism through which BRD4 drives GM-CSF-dependent TAMs activation and immune evasion in TNBC. Targeting BRD4 in combination with GM-CSF blockade represents a promising therapeutic strategy to overcome immune resistance in this aggressive breast cancer subtype.

This study reveals the ATG4B-PKM2 axis as a critical regulatory node linking autophagy, metabolic reprogramming, and EMT. Targeting this axis with Curcumol provides a precise strategy to interrupt metabolism-phenotype coupling, offering a mechanistically grounded and translationally promising approach for inhibiting CRC progression and metastasis.

In contrast, SiHa spheroids represented selective responses: MSC-exosome pretreatment did not enhance sensitivity to paclitaxel-cisplatin but improved responsiveness to paclitaxel-carboplatin, particularly within the spheroid core. Overall, MSC-exosome pretreatment exerts cell type and drug-specific effects in CC spheroids, supporting their potential to modulate chemotherapy response.

Clinically, low hsa-circ-0001030 expression correlated with advanced tumor-node-metastasis stage, poor differentiation, and unsatisfying prognosis in TSCC patients. Hsa-circ-0001030 acted as a tumor-suppressive circRNA that might depress PKM2-dependent metabolic reprogramming and cisplatin resistance in TSCC, highlighting its potential as a prognostic biomarker and therapeutic target for overcoming chemoresistance.

Cop ameliorates IR by targeting SMARCE1-mediated suppression of glycolytic flux. These findings elucidate both the mechanistic basis and therapeutic potential of Cop for the treatment of metabolic disorders.

Nitrosative stress can promote the malignant biological behavior of breast cancer cells through the glycolytic pathway.

These findings collectively demonstrate that PTBP1 is overexpressed in BC and drives cancer-specific metabolic reprogramming associated with the Warburg effect. Therefore, PTBP1 may act as an oncogenic regulator of breast cancer metabolism and serve as a potential therapeutic target.

Our study uncovers a "C1orf35-driven" energy metabolism model in MM cells, providing new insights into the pathogenesis of MM and a potential novel target for the treatment of cancer cells with a high"C1orf35-driven" anabolic metabolism. Schematic diagram of C1orf35 simultaneously promotes glycolysis and OXPHOS.