ALOXE3 (Arachidonate Lipoxygenase 3)

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.

RSL3-induced ROS accumulation activated ERK/JNK signaling, upregulating downstream ATF3 expression. ATF3 transcriptionally activated ALOXE3, promoting PUFA synthesis to enhance ferroptosis susceptibility in HCC and overcome sorafenib resistance.

ALOXE3 promotes tumor progression in COAD through activation of the ERK1/2 signaling pathway and exhibits a strong association with the immune cell infiltration of the tumor microenvironment. It may serve as a prognostic biomarker and a potential therapeutic target in COAD. Further studies are warranted to validate its clinical applicability and explore its role in immunotherapeutic approaches.

This study identified three key genes that predict chemoradiotherapy sensitivity and prognosis and are involved in multiple tumor-related biological processes in ESCC. These findings provide predictive biomarkers for chemoradiotherapy response and support the development of individualized treatment strategies for ESCC patients.

Fer-1, GSH and Vitamin C attenuated the effects but not erastin...Similarly, it significantly increases the expression of SAT1, ALOX5, ALOX15, ALOXE3 and CHAC1 that, promoting ferroptosis while downregulating the NFE2L2 gene and protein that inhibit ferroptosis. SBFI26 leads to cellular accumulation of fatty acids, which triggers excess ferrous ions and subsequent lipid peroxidation for inducing ferroptosis.

Furthermore, the study demonstrated that the molecular inhibitor hesperidin, targeting TRIB3, not only reduced cell malignancy but also induced ferroptosis, thereby suppressing tumor growth. Overall, our findings unequivocally validate the proposition that TRIB3 deficiency precipitates the iron death mechanism, thereby indicating that the strategic targeting of TRIB3 could emerge as an innovative therapeutic strategy for HNSCC.

Low NOX4 levels were more favorable to patient outcomes. Our findings may facilitate future clinical diagnoses and outcome assessments of CRC.

A risk model based on lipid metabolism-related genes may predict prognosis and immunotherapeutic response in colon cancer. CYP19A1-catalyzed estrogen biosynthesis promotes vascular abnormality and inhibits CD8 T cell function through the upregulation of PD-L1, IL-6 and TGF-β via GPR30-AKT signaling. CYP19A1 inhibition combined with PD-1 blockade represents a promising therapeutic strategy for colon cancer immunotherapy.

Based on multi-dimensional analyses, we characterized ferroptosis, probable core genes, and the upstream regulators in human CRC. The findings here may improve our understanding of ferroptosis in CRC and provide new opportunities for clinical diagnosis and treatment.

ZIC2 expression was correlated with immune-cell infiltration. These risk genes, interaction networks, and enrichments may provide a better understanding of the complex molecular mechanisms in COAD development and potential therapeutic targets for clinical treatment of COAD.

This study constructed a potential prognostic model of LCRC and RCRC, respectively. We also identified the crucial pathways that contribute to elucidating the pathogenesis of CRC.