# Roles of nucleotide metabolism in pancreatic cancer

**Authors:** Quanlin Liu, Jiahua Liu, Shige Wang, Nabuqi Bao, Xinya Zhao, Lei Wang

PMC · DOI: 10.3389/fimmu.2025.1637768 · 2025-10-22

## TL;DR

This paper reviews how nucleotide metabolism influences pancreatic cancer development and explores potential therapeutic targets to improve patient outcomes.

## Contribution

The paper emphasizes recent advancements in understanding nucleotide metabolism in pancreatic cancer and highlights novel diagnostic and therapeutic strategies.

## Key findings

- Disruptions in nucleotide metabolism contribute to tumor proliferation and chemotherapy resistance in pancreatic cancer.
- Targeting enzymes like RRM2 and TS, or pathways like PI3K/AKT/mTOR, shows promise in reducing tumor growth and inflammation.
- Recent studies identify nucleotide metabolic pathways as potential therapeutic targets for pancreatic cancer treatment.

## Abstract

Nucleotide metabolism plays a pivotal role in the onset and progression of various human diseases, including pancreatic disorders. As fundamental biomolecules, nucleotides are essential for DNA and RNA synthesis, energy production, and cell signaling. Disruptions in nucleotide metabolic pathways have been linked to altered cell proliferation, apoptosis, and immune responses—critical processes in the development of pancreatic diseases. In pancreatic cancer, metabolic changes in nucleotides facilitate rapid tumor cell proliferation and enhance chemotherapy resistance. Recent studies have concentrated on identifying specific enzymes and pathways within nucleotide metabolism as potential therapeutic targets. Targeted interventions, such as modulating RRM2, TS, and other key enzymes or disrupting the PI3K/AKT/mTOR pathway, have demonstrated potential in reducing tumor growth and inflammation in pancreatic tissue. This review provides an overview of the latest advancements in the understanding of nucleotide metabolism in pancreatic cancer pathogenesis, emphasizing diagnostic and therapeutic strategies that may improve patient outcomes.

## Linked entities

- **Genes:** RRM2 (ribonucleotide reductase regulatory subunit M2) [NCBI Gene 6241], CACNA1C (calcium voltage-gated channel subunit alpha1 C) [NCBI Gene 775]
- **Diseases:** pancreatic cancer (MONDO:0005192)

## Full-text entities

- **Genes:** AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, RRM2 (ribonucleotide reductase regulatory subunit M2) [NCBI Gene 6241] {aka C2orf48, R2, RR2, RR2M}
- **Diseases:** pancreatic cancer (MESH:D010190), tumor (MESH:D009369), inflammation (MESH:D007249), pancreatic disorders (MESH:D010195), pancreatic diseases (MESH:D010182)
- **Chemicals:** Nucleotide (MESH:D009711)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12585966/full.md

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Source: https://tomesphere.com/paper/PMC12585966