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Poster Display & Cocktail

96P - Exploiting metabolic reprogramming via targeting novel genetic variant in urocanate hydratase 1 in histidine catabolism as a potential therapeutic approach in the treatment of colorectal cancer

Date

03 Mar 2025

Session

Poster Display & Cocktail

Presenters

Amir Avan

Citation

Annals of Oncology (2025) 10 (suppl_2): 1-9. 10.1016/esmoop/esmoop104255

Authors

A. Avan1, H. Azari2, H. Ibrahim Alshekarchi2, G.J. Peters3, G.A. Ferns4, E. Giovannetti5

Author affiliations

  • 1 Biomedical Sciences, Queensland University of Technology, 4000 - Brisbane/AU
  • 2 Metabolic Syndrome Research Center, Mashhad University of Medical Sciences, 99191-91778 - Mashhad/IR
  • 3 Medical Oncology Dept, Amsterdam UMC, locatie VUmc, 1081 HZ - Amsterdam/NL
  • 4 Metabolic Syndrome Research Center, Surrey and Sussex Cancer Alliance, GU2 7YG - Guildford/GB
  • 5 Medical Oncology Dept, Amsterdam UMC - Vrije University Medical Centre (VUmc), 1081 HV - Amsterdam/NL

Resources

This content is available to ESMO members and event participants.

Abstract 96P

Background

Colorectal cancer (CRC), is second leading causes of cancer-related deaths. Hence there is an imperative need for the identification of new therapeutic targets. This study aimed to identify genetic variants using genome-wide DNA and RNA sequencing and Pan-Cancer Studies followed by validation cohort & functional analyses.

Methods

RNAseq/DNAseq were used in 146 patients. Gene Ontology, Reactom, Human Disease Ontology were employed. Survival analysis was conducted. The candidate genes were subjected to machine learning-based analysis and ROC. The expression was evaluated by RT-PCR in110 cases. Gene variants were further validated followed by Whole Exome Sequencing in 15 patients. We performed functional analyses in CRC cells via knock down by PIKOI vector for Urocanate Hydratase 1 (UROC1) in cells (CT26-SW480) and then performed Proliferation, 3D Spheroid Model, Cell cycle perturbation, RT-PCR/ELISA and LC-MS/MS.

Results

A total of 2985 DEGs in the advanced stages were identified. Histidine pathway and UROC1 gene were identified as potential prognostic marker. The UROC1 was sensitive, with an AUC of 0.934. The expression levels of the gene were higher in patients. Moreover, our data identified a novel genetic variant in UROC1. ROC curve analysis indicated that UROC1 possesses 70% diagnostic potential, which its value was enhanced by KRAS/NRAS/APC. Functional enrichment analysis underscores the involvement of UROC1 in tumor progression. The prognostic assessment indicates that elevated UROC1 expression correlates with adverse outcomes across multiple GI. Genetic alteration analysis highlights the prevalence of mutations, particularly missense mutations, in UROC1. Significant correlations between UROC1 expression and immune cell infiltration and histidine pathway are observed, suggesting its involvement in tumor immune evasion mechanisms, while its modulation reduces cell growth in CRC cells.

Conclusions

Our study is a world-first, to explore how cancer cells manipulate CRC progression via histidine alterations. Our data illustrated the potential value of UROC1, novel identified variant, rs751617501 in advanced-CRC patients.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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