ODC1 (Ornithine Decarboxylase 1)

Additionally, in a Dextran Sulfate Sodium (DSS)-induced colitis model combined with single-cell RNA sequencing, PUT supplementation resulted in the elimination of CXCR6+ CD8+ T cells in the colon. These findings provide new insights into how polyamine metabolism, particularly involving extracellular PUT, impairs the anti-tumor activity of CXCR6+CD8+ T cells, potentially contribut ing to CRC progression.

Oleic acid-HOXB9-ODC1 stable cascading axis then is confirmed in patient tissues, and ODC1 inhibitors boost patient-derived tumor cells' chemosensitivity. This study links fatty acids to polyamine buildup, reveals a mechanism for metabolic syndrome-driven endometrial cancer, and points to HOXB9 and ODC1 as potential therapeutic targets.

Gene-set enrichment analyses linked high ODC1 expression to MYC target signatures, positioning ODC1 as a clinically relevant, AR-regulated oncogenic node that integrates germline risk with core prostate cancer circuitry. IP-SNPs-seq thus provides a scalable route from association to mechanism, broadly applicable to diverse TFs and diseases, and nominates the AR-rs7600820-ODC1 axis as a potential biomarker and therapeutic vulnerability in androgen-driven prostate cancer.

Treatment with an ODC1 selector inhibitor mitigates CSC enrichment, sensitizes tumors to cisplatin, and restricts tumor regrowth. Together, the study shows that efferocytosis and associated polyamine metabolic reprogramming support the chemotherapy-induced enrichment of CSCs, providing new targets for addressing chemoresistance and recurrence of OC.

These findings illuminate the critical role of apoptotic cell metabolites in mediating treatment resistance and suggest that targeting SPD may offer a promising therapeutic strategy to augment the effectiveness of chemotherapy in OS.

Targeted re-analysis of publicly available single-cell RNA-sequencing datasets from COVID pneumonia patients revealed elevated CDC6 expression alongside reduced MYC and ODC1 levels in alveolar epithelial cells exhibiting markers of senescence. Collectively, these findings identify putrescine as a metabolic checkpoint in replication stress-induced senescence and reveal a MYC-orchestrated signaling-metabolic circuit that temporally integrates oncogene activation with cell fate decisions.

By targeting the RBBP5/KAT2B epigenetic modification complex, HClnc1 increases ODC1 promoter activity to enhance ODC1 transcription and promote the proliferation and migration of liver cancer cells.

Developing more potent inhibitors with improved drug-like properties is crucial for advancing polyamine- targeted therapies and positioning this field at the forefront of cancer research.

Importantly, ODC1 overexpression and positive immunostaining correlated with significantly worse overall survival (p < 0.05). These results indicate that ODC1 overexpression and positive immunostaining are associated with poor prognosis in PSCC, supporting ODC1's value as a prognostic biomarker and highlighting its potential as a novel therapeutic target, given available anti-cancer drugs targeting ODC1 activity.

There is a growing number of laboratories that have become interested in exploring polyamines (in part due to metabolomics analyses in human health-related studies). The detailed protocols of this chapter provide step-by-step guidance detailing how to measure ODC activity and polyamines in human RBCs.

Our study effectively advances the precise risk stratification of DLBCL and reveals that ODC1 and immune-deserted microenvironment jointly shape a group of DLBCL patients with stem cell-like features. Targeting ODC1 regulates immunotherapies in DLBCL, offering new insights for DLBCL treatment.

A novel specific HIF-1 inhibitor britannin is identified through a natural compound library screening, and demonstrate that coadministration of britannin efficiently inhibits chemotherapy-induced HIF-1 transcriptional activity, ODC1 and SRM expression, polyamine levels, and BCSC enrichment in vitro and in xenograft and autochthonous mouse models. The findings demonstrate the key role of polyamine anabolism in BCSC regulation and provide a new strategy for breast cancer treatment.