ACOX1 (Acyl-CoA Oxidase 1)

Crucially, the HSP90AB1 K265R mutation or pharmacological inhibition of ACOX1 (10,12-tricosadiynoic acid) or TXN (1-methyl-propyl 2-imidazolyl disulfide, PX-12) synergizes with cisplatin to suppress tumor growth in vivo by disrupting redox adaptation. These findings reveal that crotonylation is a hypoxia-sensitive rheostat for TXN-mediated redox control, suggesting that the ACOX1-HSP90AB1-TXN axis is a therapeutic vulnerability in therapy-resistant OSCC.

Based on the experimental results, we have determined that bile-derived liver organoids are well-suited for constructing an in vitro disease model of hormone-induced lipid metabolism abnormalities, enabling effective observation of lipid phenotypes. Furthermore, we have screened and identified lncRNAs involved in hormone-regulated lipid metabolism abnormalities at the non-coding regulatory level. These findings offer potential diagnostic markers and therapeutic targets for disorders related to lipid metabolism.

Among 17 patients in the DLBCL group, 6 received epirubicin chemotherapy with an average dose of 59.28 ± 12.54 mg/m2 per cycle, and 11 received liposomal doxorubicin chemotherapy with an average dose of 25.21 ± 3.14 mg/m2 per cycle...Alterations of myocardial metabolism monitored by 18F-FDG PET/CT may represent early indicators of metabolic remodeling, potentially identifying patients at risk for AIC. https://www.chictr.org.cn/, identifier ChiCTR2400088740.

Our findings identify the FABP1/PPARγ axis as a central regulator of peroxisome-centered FAO and redox buffering in cetuximab-tolerant DTP cells. Targeting FABP1 collapses this adaptive metabolic-redox program, restores vulnerability to oxidative stress, and alleviates immune suppression, highlighting peroxisomal lipid metabolism as a therapeutically actionable vulnerability in refractory HNSCC.

Consistently, BAP31 knockdown amplified ethanol-induced lipid accumulation, inflammation, impaired glycogen storage, ER stress, and suppression of Pparα signaling in HepG2 cells. Together, these findings demonstrate that BAP31 deficiency exacerbates ethanol-induced liver steatosis, inflammation, and liver injury by impairing fatty acid oxidation and glycogen synthesis, and by amplifying ER stress responses.

In vivo, atorvastatin markedly reduced CRA burden in AOM-DSS-induced mouse model, particularly demonstrating enhanced efficacy in high-fat diet contexts. This translational study establishes atorvastatin's dual mechanism in metabolic reprogramming and stemness inhibition, suggesting its potential as a therapeutic strategy for CRA prevention and treatment.

AC is characterized by distinct metabolic reprogramming, with preferential upregulation of peroxisomal β-oxidation rather than mitochondrial pathways. These metabolic features are accompanied by a high prevalence of activating PIK3CA mutations, suggesting a link between genomic alterations and metabolic phenotype. These findings provide new insights into the pathobiology of AC and may assist in its histopathological differentiation from other breast cancer subtypes.

Instead, it promoted the upregulation of fatty acid oxidation-related genes such as Peroxisome proliferator-activated receptor alpha (PPARα) and Acyl-CoA oxidase 1 (Acox1), helped maintain intestinal microbial balance, and enhanced the production of beneficial short-chain fatty acids (SCFAs), particularly butyrate and propionate. In conclusion, solvent fractionation effectively modulates the fatty acid composition of sheep fat, thereby influencing lipid metabolism and inflammatory responses through the regulation of key gene expression and modulation of the gut microenvironment.

Our findings uncover a novel mechanism by which DDX1 crotonylation regulates the AS of peroxisome-related genes and mediates peroxisomal redox homeostasis. This discovery bridges a critical gap in our understanding of how posttranslational modifications (PTMs) of DEAD/DEXD box RNA helicases modulate gene AS and identifies a potential therapeutic target for colorectal cancer.

Our results elucidates the key pathway through which high CLIC1 expression enhances cellular oxidative stress, subsequently promoting gastric cancer progression. Therefore, CLIC1 might function as a redox regulation therapy target and a tumor marker.

High expression of YEATS4 fortifies fatty acid metabolism, enhances self-renewal and growth of ALDH+ breast cancer stem cells, and is correlated with poor prognosis of breast cancer patients, especially the ER+ subtype. Our work uncovers YEATS4 as an "amplifier" in the feedforward circuit of histone crotonylation and lipid metabolism underlying the stemness and cell proliferation, supporting the pursuit of YEATS4 as a potential target for breast cancer intervention.

All our findings provide hypotheses for PFOS/PFOA-induced tumorigenesis; however, experimental studies are required to establish translational relevance. All the R codes developed in this study are publicly available.