LOX (Lysyl Oxidase)

Molecular mechanics/generalized Born surface area (MM/GBSA) analysis supported strong protein-ligand interactions, whereas in silico absorption, distribution, metabolism, excretion, and toxicity (ADMET) evaluation indicated desirable pharmacokinetic and safety profiles. These findings highlight the identified resveratrol derivatives as promising dual COX-2/5-LOX inhibitors for further development in cancer therapy.

Collagen fiber density/alignment and MYC/AP-1 gene signatures served as pharmacodynamic readouts of drug activity. These data uncover a tractable ECM-integrin-MYC axis in ILC and nominate PXS-5505, alone or with endocrine therapy, for window of opportunity trials in this understudied breast cancer subtype.

While mitogen-activated protein kinase kinase (MEK) inhibitors, selumetinib and mirdametinib, can reduce tumor volume, surgical resection remains the primary treatment for immediate debulking and symptom relief. These results provide the first evidence that ECM stiffening, such as that arising from postsurgical remodeling, directly drives pNF1 progression and therapeutic resistance. Our findings highlight mechanobiology as a key regulator of tumor behavior and support targeting ECM mechanics to improve clinical outcomes in NF1 patients.

Drug sensitivity screening identified six small molecules (PD0325901, ERK-6604, paclitaxel, ribociclib, TAF1, and lapatinib) that targeted SLC12A5-related pathways. Crucially, multivariate Cox regression analysis confirmed that SLC12A5 was an independent prognostic factor (HR p = 0.04). This study established SLC12A5 as a novel biomarker for GBM, uniquely bridging molecular dysregulation, edema pathogenesis, and radiomics with implications for prognosis and targeted therapy.

Oral administration of ENHL selectively colonizes tumors, where arabinose induction triggers localized LOx expression, significantly improving radiosensitivity and immune cell infiltration while modulating gut microbiota. This synergistic approach-combining targeted metabolic modulation with microbial precision therapy-represents a transformative strategy to overcome RT resistance in colorectal cancer, offering a promising pathway toward clinical translation.

Flavonoids are promising ferroptosis inducers for apoptosis-resistant cancers, leveraging multi-target mechanisms and emerging delivery technologies. Future research should prioritize clinical translation, biomarker identification, and optimized combination regimens to enhance therapeutic outcomes.

Experimental validation confirmed significantly elevated expression of these three genes in GBM cells compared to normal controls. The cuproptosis-related genes VEGFA, LOX, and LOXL1 are highly expressed in GBM and closely associated with tumor progression and poor prognosis, suggesting their potential as core biomarkers for GBM diagnosis, therapy, and prognosis evaluation.

We found that negativity for LOXL2 expression was an indicator of higher risk of death due to the disease. Our results suggest that lysyl oxidases such as LOXL2 are potential prognostic markers in mammary carcinomas of dogs.

In xenograft models of ovarian and triple-negative breast cancer, VPA significantly improved tumor control and survival without added toxicity. These findings support metabolic-epigenetic modulation as a strategy to improve CAR-T therapy in solid tumors.

report the identification of two transcriptionally distinct renal cell carcinoma tumor thrombus subtypes. The aggressive TT1 subtype is characterized by LOX-expressing cancer cells within an immunosuppressive microenvironment dominated by THBS2+ fibroblasts and GPNMB+ macrophages that exclude CD8+ T cells.

Mechanically, hypoxia-activated HIF-1α/LOX signaling promoted ITGA5/FN1-dependent extracellular matrix remodeling and contributed to a chemoprotective niche. This vascularized 3D lung cancer model offers a physiologically relevant and translationally valuable platform for investigating non-small cell lung cancer progression and optimizing patient-specific drug screening.

ARA metabolic dysregulation contributes to COPD pathogenesis, and (±)12-HETE, 15(S)-HETE, and (±)11-HETE may serve as potential biomarkers for COPD. MLWE exert therapeutic effects by modulating ARA metabolism, ameliorating oxidative stress, and suppressing inflammatory responses, offering a novel strategy for COPD prevention and treatment.