ALOX5 (Arachidonate 5-Lipoxygenase)

In vivo studies using a nude mouse model demonstrated that TEC inhibits tumor growth and downregulates ALOX5, 5-HETE, and PD-L1 expression in tumor tissues. The findings suggest that the ALOX5/5-HETE signaling pathway is crucial for regulating lipid metabolism and ferroptosis in ovarian cancer, and TEC may exert its anti-tumor effects, at least in part, by modulating this pathway (The graphical abstract was shown in Fig. 1).

These events increase lipid peroxidation and ferroptosis susceptibility in hematopoietic cells as evidenced by enhanced BODIPY-C11 oxidation and erastin sensitivity. Our findings reveal a spliceosome-to-chromatin-to-metabolism pathway in which SF3B1 mutations promote ferroptosis through BRD9-mediated chromatin dysregulation, highlighting the previously unrecognized metabolic rewiring in myeloid malignancies.

Tumor-intrinsic ALOX5 is a novel tumor suppressor that orchestrates CD8⁺ T infiltration via the AA-LTB4 axis in NSCLC. Our findings establish ALOX5-mediated AA metabolism as a therapeutically targetable pathway to overcome immunotherapy resistance, positioning dietary AA supplementation as a promising adjunctive strategy.

Chemotherapy remains the cornerstone of gastric cancer (GC) treatment, with Oxaliplatin (OXA) being a critical first-line agent...These findings suggest that JMJD3 plays a pivotal role in GC chemoresistance by modulating both stemness and ferroptosis sensitivity. Targeting JMJD3 may provide a novel therapeutic strategy for overcoming chemotherapy resistance, with ferroptosis inducers potentially offering a promising adjunctive treatment in GC.

In this pilot study, HCC and liver metastases demonstrated fundamentally different spatial architectures, with metastases uniquely harboring a germline/neural-like plasticity hub. Despite these organizational contrasts, both tumor types converged on a shared program of metabolic rewiring, highlighting potential therapeutic targets that link local tumor niches to systemic host-tumor interactions.

Isopimpinellin inhibits macrophage M1 polarization in cancer tissues and M2 polarization in para-carcinoma tissues by targeting ALOX5, thereby inhibiting tumor growth and inflammatory response in CAC mice. This study provides strategies for the treatment of CAC.

ALOX5 overexpression promoted the release of LDH, PI-positive cells, pyroptosis related protein expression, oxidative stress and inflammatory cytokine release induced by Ang II in MA-VSMCs, while they were reversed by BAY11-7082 (BAY, NF-κB inhibitors)...The addition of NF-κB pathway inhibitor BAY inhibited the increase of inflammatory factors and pyroptosis caused by ALOX5 overexpression. These results indicated that ALOX5 promoted pyroptosis through NF-κB pathway, and then promoted AAA development.

Further animal experiments confirmed that BC/GD combination therapy could effectively improve brain tissue pathological damage, and its protective effects are closely associated with the regulation of lipid metabolism disorders and inflammatory responses. These findings highlight ALOX5AP as a key molecular mediator in CSVD pathogenesis and support BC/GD as a promising dual-target therapeutic strategy for the treatment and prevention of CSVD.

Further in vivo and in vitro experiments demonstrated that dexrazoxane (DXZ) could ameliorate DIC caused by Alox5 overexpression by alleviating ferroptosis. Our study showed that the downregulation of Alox5 alleviated myocardial damage associated with DIC via the P53/SLC7A11 pathway. Therefore, inhibiting Alox5 might be a potential strategy for the treatment of DIC.

Perillaldehyde attenuated IL-1β-induced mitophagy-associated apoptosis and NLRP3-mediated inflammation through decreasing ALOX5 and inactivating NF-κB signaling, indicating the potentially protective potential of perillaldehyde in osteoarthritis.

In this study, ADH1A, ACACB, CD36, CERS4, PDE3B, ALOX5, and CRAT were identified as biomarkers for PC, with their expression levels validated in clinical samples. These findings offered a potential theoretical foundation for developing targeted treatments for PC.

The RS output by the LR model strongly correlated with ALOX5 expression (P<0.05). The findings suggest that evaluating ALOX5 expression using a radiomics model to predict the clinical prognosis of NSCLC patients could have potential clinical applications.