ALOX15B (Arachidonate 15-Lipoxygenase Type B)

This study constructed and validated a metabolism-driven prognostic model. The model enables prognostic stratification of LGG patients and links high-risk scores to metabolic dysregulation and an immunosuppressive microenvironment characterized by M2 macrophage enrichment, based on multi-omics data. Mechanistic exploration indicates this association is particularly pronounced in myeloid cells, predominantly within metabolism-related M2 macrophage subpopulations. Furthermore, computational analysis suggests differences in drug sensitivity between risk groups and identifies potential therapeutic compounds, providing clues for future exploration of therapeutic strategies targeting metabolic-immune interactions.

These findings provide preliminary evidence supporting further investigation of sex-specific approaches to BC management.

Mammalian ALOX15 orthologs are allosteric enzymes but the molecular basis for their allosteric properties remains controversial. In fact, two alternative hypotheses (presence of allosteric binding sites at enzyme monomers vs. ALOX15 dimers consist of an allosteric and a catalytic monomer) have been introduced and this review is aimed at critically evaluating the pros and conts of these two mechanistic scenarios.

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.

Functional studies were conducted by overexpressing or knocking down ALOX15B in TNBC cells treated with erastin (a ferroptosis inducer)...Collectively, our study suggests that IRF1 transcriptionally activates ALOX15B to enhance ferroptosis sensitivity in TNBC cells. These findings provide new insights into the molecular mechanisms underlying TNBC progression and suggest potential therapeutic targets for TNBC treatment.

This study identified ALOX15B, TIAM1, and TMC6 as potential risk genes and JUN, PAPSS2, and RAP1GAP as protective genes in THCA. These genes may serve as promising biomarkers and therapeutic targets for THCA, offering novel insights into precision oncology.

Notably, treatment with methyl protodioscin (MPD), a steroid saponin primarily purified from polygonatum sibiricum rhizome, restored the S-palmitoylation and membrane location of ALOX15B via disruption of the ABHD17C/ALOX15B interaction, consequently resulting in significant inhibition of growth rate of patient-derived KRASmut-PDAC organoids in vitro and KRASmut-PDAC-formed tumor in vivo via induction of ferroptosis. Therefore, these findings unveil a prominent role of ferroptosis evasion in KRASmut-PDAC progression and highlight the potential of targeting KRAS/ERK1/ABHD17C/ALOX15B axis in KRASmut-PDAC treatment.

Efferocytosis-related models can be used for the assessment of breast cancer prognosis, while the efferocytosis-related gene ALOX15B can affect the migration and invasive ability of breast cells.

BML and IVL exhibit distinct gene mutations in tumor development, with certain shared mutations.

These findings provide critical insights for drug development efforts. This study elucidates the therapeutic potential of Licochalcone D, a traditional Chinese medicine monomer, in improving sepsis through the regulation of ferroptosis, thereby providing a new direction and option for subsequent clinical drug development in the treatment of sepsis.

Furthermore, plasma membrane lipids were investigated via confocal microscopy, revealing reduced cholesterol and lipid rafts. This study suggests a role for ALOX15B in keratinocyte inflammation through modulation of lipid peroxidation and the EGFR/JAK1/STAT1 signalling axis.