# Purinergic Signaling in Ovarian Carcinoma

**Authors:** Angélica Sofía Martínez-Ramírez, José David Nuñez-Ríos, Ana Patricia Juárez-Mercado, Anaí del Rocío Campos-Contreras, Francisco G. Vázquez-Cuevas

PMC · DOI: 10.34172/apb.025.46032 · Advanced Pharmaceutical Bulletin · 2025-10-25

## TL;DR

This review explores how purinergic signaling contributes to ovarian carcinoma and highlights its potential as a target for new therapies.

## Contribution

The paper provides a comprehensive overview of purinergic signaling's role in ovarian carcinoma and its therapeutic potential.

## Key findings

- Purinergic signaling promotes tumor growth and metastasis in ovarian carcinoma.
- Adenosine suppresses anti-tumor immune responses through interactions with immune cells.
- Purinergic elements are potential targets for novel ovarian carcinoma therapies.

## Abstract

Ovarian carcinoma (OC) is the most lethal gynecological cancer worldwide. Around 95% of patients exhibit recurrence five years after treatment; 80% experience recurrence within 18 months after first-line treatment, and progression-free survival rates have not changed over the past 40 years. New therapeutic approaches are imperative to face this complex disease. The purinergic system is a newly recognized element of the tumor microenvironment (TME), as it exhibits a pro-tumor role. Tumor cells release adenosine triphosphate (ATP) into the TME, where it exerts autocrine-paracrine actions that regulate several processes, including the induction of a metastatic phenotype, cell proliferation, and metabolic adaptations. In the extracellular milieu, ATP is converted to adenosine (ADO) by ectonucleotidases (CD39 and CD73), thereby significantly blocking the anti-tumor immune response through interactions with various immune cells. Recent analyses have focused on the diversity and plasticity of purinergic signaling in OC. This review outlines the disease, explains basic concepts of purinergic signaling, and summarizes experimental evidence that indicates purinergic elements may serve as potential targets for novel therapies to overcome OC.

## Linked entities

- **Proteins:** ENTPD1 (ectonucleoside triphosphate diphosphohydrolase 1), NT5E (5'-nucleotidase ecto)
- **Chemicals:** adenosine triphosphate (PubChem CID 5957), adenosine (PubChem CID 60961)
- **Diseases:** ovarian carcinoma (MONDO:0005140)

## Full-text entities

- **Genes:** NT5E (5'-nucleotidase ecto) [NCBI Gene 4907] {aka CALJA, CD73, E5NT, NT, NT5, NTE}, ENTPD1 (ectonucleoside triphosphate diphosphohydrolase 1) [NCBI Gene 953] {aka ATP-DPH, ATPDase, CD39, NTPDase-1, SPG64}
- **Diseases:** OC (MESH:D010051), Tumor (MESH:D009369)
- **Chemicals:** ATP (MESH:D000255), ADO (MESH:D000241)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12980269/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12980269/full.md

## References

70 references — full list in the complete paper: https://tomesphere.com/paper/PMC12980269/full.md

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Source: https://tomesphere.com/paper/PMC12980269