ALDOA (Aldolase Fructose-Bisphosphate A)

Additionally, farnesol impaired mitochondrial ATP synthesis by reducing mitochondrial membrane potential (MMP) to 66% and elevated ROS levels to 54% creating a disturbance in mitochondrial stability. Overall, Farnesol significantly disrupts anaerobic glycolysis in A549 cells promoting cell death through mitochondrial dysfunction, oxidative stress, apoptosis and reducing cellular acidosis.

This study identified the basis for the synergistic effect of ginger juice on EC and supported the scientific rationale for G-EC processing. In this study, CFA improved OA by affecting glycolysis and modulating lactylation at the H3K23la site of H3 histones, highlighting the critical role of CFA in its anti-OA effects. A non-invasive diagnostic model for OA was developed, which facilitated the rapid prediction of OA risk in patients, and interpretable machine-learning methodologies enabled the analysis of key metabolic markers.

Our study identifies a novel, non-enzymatic function of ALDOA as a critical regulator of lysosomal degradation of macropinocytosed proteins via interaction with V-ATPase. This mechanism is essential for metabolic adaptation and growth of KRAS-mutant tumors under stress conditions. Targeting ALDOA offers a promising therapeutic strategy for cancers that rely on extracellular nutrient scavenging.

A Kla-high transcriptional signature shortens median overall survival by 18 months and stratifies patients with poor response to sorafenib and immune checkpoint blockade. Three convergent therapeutic entry points emerge: depletion of lactate via glycolytic inhibition or MCT1/4 blockade (FX11, AZD3965), enzymatic modulation of Kla writers or erasers, and PROTAC-mediated degradation of oncogenic lactylated proteins. In murine and patient-derived xenograft models, these strategies reduce tumour volume by at least 50% and synergise durably with anti-PD-1 therapy. This integrated synthesis positions lysine lactylation as a hierarchical regulator that links metabolic stress to epigenetic plasticity, immune escape, and therapeutic vulnerability, and outlines a biomarker-driven roadmap for lactylation-targeted precision medicine in HCC.

On the other hand, it inhibits transketolase (TKT) in the PPP and aldolase A (ALDOA) in glycolysis, which blocks the supply of raw materials required for nucleic acid synthesis, thus inhibiting DNA synthesis and tumor cell proliferation. In conclusion, this study confirms that kaempferol disrupts the metabolic homeostasis of cancer cells across multiple dimensions, including energy metabolism, biosynthesis, and oxidative stress, indicating its potential for development as a novel anti-colorectal cancer drug targeting tumor metabolism.

Our findings establish ALDOA as a robust prognostic biomarker and a key regulator of macrophage-mediated immune suppression in LUSC. Its involvement in tumor metabolism, immune evasion, and therapy resistance suggests that targeting ALDOA could enhance both metabolic inhibition strategies and immune checkpoint blockade therapies. Future research should focus on mechanistic studies and therapeutic interventions targeting ALDOA to improve treatment outcomes in LUSC.

Moreover, ALDOA inhibitors selectively promote ferroptosis in cancer cells, both in vitro and in vivo. Collectively, the findings reveal that ALDOA-mediated metabolic reprogramming is a targetable vulnerability for ferroptosis sensitization in cancer.

Thiabendazole demonstrates promising anticancer potential in LUAD, influencing key genes and immune pathways. It may serve as an effective therapeutic agent targeting both cancer cells and the tumor microenvironment.

A survival prediction nomogram, constructed based on the univariate analysis of data from the Cox proportional hazard model, demonstrated that the expression of ALDOA and ENO1 significantly impacts the prognosis of GC patients. ALDOA/ENO1 may play a crucial role in GC, which may potentially offer new perspectives and directions for the development of targeted therapies specifically designed for GC patients.

Instead of broadly targeting ALDOA, which causes glycolysis impairment, the specific elimination of ALDOA ubiquitination enhances chemosensitivity and the synergistic effect of chemotherapy combined with p65-specific anti-inflammatory therapy by selectively suppressing inflammation-induced proliferation in cancer cells. Collectively, we unveil the multifaceted mechanisms by which ALDOA promotes PDAC carcinogenesis, from metabolic to gene regulatory perspectives, providing potential therapies combatting cancer.

All our findings provide hypotheses for PFOS/PFOA-induced tumorigenesis; however, experimental studies are required to establish translational relevance. All the R codes developed in this study are publicly available.

An 18-protein (PURB, SDCBP2, CD2BP2, GALM, SERPINA3, OAS3, FAN1, ZPR1, KRT2, NUDT2, SMNDC1, SERPINA4, CUTA, WDR36, POSTN, CLEC11A, PEX14, and PI4KA) risk score demonstrated independent prognostic significance for overall survival, and recurrence, and was validated in an independent proteomic dataset generated using a different proteomic technology. This study introduces four novel prognostic PDA subtypes and an 18-protein risk score, validated in an independent dataset, which show promise for improving survival prediction and could serve as a valuable tool for personalized treatment guidance.