ALOX15 (Arachidonate 15-Lipoxygenase)

Concurrently, VEGF downregulation and p53 upregulation reflected additional anti-angiogenic and pro-apoptotic effects. Collectively, the lactoferrin-functionalized Nic-NLC produced the most robust antitumor response, with superior ferroptosis induction, redox modulation, and anti-angiogenic activity.

AS601245, AP.24534 and roscovitine were the top three chemotherapeutic agents showing the highest sensitivity differences between the risk groups. The RT-qPCR results indicated that the expression of electron transfer flavoprotein subunit α, rap guanine nucleotide exchange factor-like 1, keratin 7, cluster of differentiation 24, proline rich 15-like, arachidonate 15-lipoxygenase type B, ELOVL fatty acid elongase 2 and C-X-C motif chemokine ligand 9 was consistent with the results of bioinformatic analysis. In conclusion, the HER2-related risk model and nomogram developed in the present study demonstrated high accuracy in predicting patient survival.

Similarly, SCDA also increased levels of the antioxidant glutathione (GSH), which is associated with inhibition of P53 and promotion of the expression of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), resulting in an improved balance between antioxidant and oxidant systems. This provides new drugs and targets for the treatment of right ventricular hypertrophy.

ALOX15 could exacerbates high-altitude hypoxic ALI inflammatory responses by promoting both macrophage ferroptosis and M1 polarization. Identification of baicalein as an ALOX15 inhibitor mitigates ferroptosis, shifts macrophages to the M2 phenotype, and reduces inflammation, offering a promising preventative strategy for high-altitude hypoxic lung injury.

AA induces ferroptosis in HCC through the SIRT5-ACSL4/LPCAT3/ALOX15 pathway, offering mechanistic insight into lipid metabolism-related ferroptotic regulation.

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.

The ferroptosis-related gene HSPA5 diminishes the effectiveness of LUAD immunotherapy by promoting immune evasion, thus serving as a potential indicator for predicting the therapeutic response. Notably, patients with lower HSPA5 expression tend to have a more favorable prognosis. Our discoveries may contribute significantly to the advancement of personalized treatment strategies and the enhancement of immunotherapy outcomes for LUAD patients.

In vivo and in vitro experiments were conducted using the 12-LOX inhibitor ML355 to investigate the role of the 12-LOX/12-HETE/GPR31 metabolic pathway in M2 macrophage polarization and tumor progression through flow cytometry, reverse transcription polymerase chain reaction (RT-PCR), 5-Ethynyl-20-deoxyuridine (EdU) assays, and Transwell experiments...Moreover, inhibiting 12-LOX reduced the co-cultured M2 macrophages. This study, through in vivo and in vitro experiments, reveals that the 12-LOX/12-HETE/GPR31 metabolic pathway affects the growth, migration, and invasion of PC by modulating M2 macrophage polarization patterns.

CAR-T cell therapy combined with HI-TOPK-032 is a promising novel strategy for treating MSLN-expressing solid tumours.

ACHP enhances Sorafenib's efficacy by inducing lipid peroxidation-related ferroptosis and activates Th1-type anti-tumor immune responses, synergistically suppressing HCC. The study establishes a complete evidence chain of "component characterization-mechanism verification", providing novel therapeutic targets and strategic insights for the development of combination therapy for HCC.

Our results suggest that the LMG signature may serve as a novel diagnostic tool for identifying patients with UC. Our machine-learning model may contribute to future research on the formulation of potential therapeutic strategies.

In conclusion, targeting STAT6 enhances the efficacy of celecoxib in liver cancer by suppressing AA shunting. The combination of AS1517499 and celecoxib holds promise as a novel therapeutic strategy for liver cancer.