AKR1B10 (Aldo-Keto Reductase Family 1 Member B10)

Drug-gene interaction mining mapped 78 target proteins to clinically relevant compounds, including tolrestat, alcuronium, metyrosine, and 4-phenylbutyric acid...Physicochemical and pharmacokinetic profiling further prioritised tolrestat as a computationally favourable candidate (MW = 357.35, LogP = 3.64, TPSA = 81.86 Ų), exhibiting acceptable drug-likeness, high predicted gastrointestinal absorption, and low synthetic complexity (SA = 2.34), in contrast to alcuronium (MW = 666.89, SA = 7.86), which showed multiple rule violations. Collectively, this in silico study proposes a robust diagnostic gene signature for HCC and identifies tolrestat as a promising repurposing candidate that warrants experimental validation, demonstrating the utility of integrating machine learning, network biology, and molecular simulation in translational cancer research.

AKR1B10 facilitated immune evasion of KRASG12C mutation CRLM by recruiting and reprogramming neutrophils to remodel the immunosuppressive TME, providing a potential therapeutic target for KRASG12C mutation CRLM patients.

n = 2. The Urayasu classification for ALL is considered reliable for predicting the prognosis of patients with ALL after the initial Hyper CVAD/MA remission induction therapy.

The biology-informed radiomics model based on AKR1B10 expression demonstrates strong prognostic performance in hepatocellular carcinoma. By directly linking imaging phenotypes to a key molecular driver of HCC, this approach provides a clinically applicable and biologically interpretable tool for pre-operative risk prediction.

ADMET profiling confirmed SFN's high intestinal absorption and blood-brain barrier non-permeability. Thus, integrating SFN as a natural AKR1B10 inhibitor into ER-negative BC treatment regimens may enhance early malignancy management and support its development as a nutraceutical adjunct.

AKR1B10 confers lenvatinib resistance by enhancing aerobic glycolysis in HCC cells. AKR1B10 undergoes AARS1-mediated lactylation at K173, stabilizing it by antagonizing ubiquitin-proteasomal degradation. AKR1B10 promotes LDHA Y10 phosphorylation, boosting lactate production, which drives H3K18la-mediated transcriptional upregulation of LDHA, creating a feed-forward loop. Targeting AKR1B10 with epalrestat synergizes with lenvatinib to overcome resistance in preclinical models.

This integrative ML-MR framework identified CHRDL1 as a robust diagnostic and functionally relevant biomarker for NSCLC. These findings offer insights into the immune-proliferative landscape of NSCLC and provide a foundation for early detection and targeted therapy strategies.

High-risk HCC responded poorly to sorafenib and transarterial chemoembolization (TACE) but sensitively to agent ABT-263 in silico, in vitro, and in vivo experiments. Interpretability analysis revealed consistent biomarker contributions in both signatures. Conclusively, the dual signatures show promise for HCC risk stratification, pending external validation.

These findings highlight key molecular differences in HCC across ethnicities and emphasize the value of TCGA data for identifying both shared targets and population-specific therapeutic strategies. Understanding these differences is crucial for advancing precision oncology and developing tailored interventions.

Flexibility of the complementarity-determining region loops in 4B5 imparts paratope plasticity that enables interaction with AKR1B family proteins. This antibody off-target recognition can result in cytoplasmic and nuclear IHC staining.

Among the identified candidates, miR-423-5p, AKR1B10, and 3-methylhistidine provide the most robust evidence. Future multicenter, longitudinal studies with standardized protocols and validation are essential.

Quantum mechanical analysis indicated favourable electronic properties and chemical stability. These results suggest that Ezetimibe is a selective and stable AKR1B10 inhibitor, warranting further investigation for drug-resistant cancer therapy.