PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
May 27, 2026Purinergic Signalling0 citationsOpen Access

Nucleotide signaling in neutrophils: a key player in cancer dynamics

JSJean Lucas Gutknecht da SilvaJSJean SévignyDLDaniela Bitencourt Rosa Leal

Key Points

  • This review aims to explore the role of nucleotide signaling in regulating neutrophil responses and its implications for cancer dynamics.
  • Summarized findings from recent research on neutrophil functions and nucleotide signaling.
  • Discussed the impact of neutrophil heterogeneity on cancer progression.
  • Highlighted therapeutic strategies to modulate neutrophil activity via nucleotide signaling.
  • Extracellular nucleotides regulate key neutrophil functions such as adhesion, chemotaxis, and degranulation.
  • Neutrophil heterogeneity affects tumor progression through both pro- and antitumor effects.
  • Targeting nucleotide signaling may provide novel therapeutic approaches for cancer treatment.

Abstract

Neutrophils are key innate immune cells whose effector mechanisms are increasingly recognized as therapeutic targets in chronic inflammation and cancer. While highly heterogeneous and functionally versatile, they can also exacerbate inflammation and tissue damage, making precise modulation critical for homeostasis. Nucleotide signaling-including extracellular nucleotide-metabolizing enzymes and receptors for ATP, UTP, and adenosine-plays a central role in regulating neutrophil responses. Extracellular nucleotides influence adhesion, chemotaxis, and degranulation, with important implications in cancer. Neutrophil heterogeneity affects tumor progression through both pro- and antitumor mechanisms. This review summarizes these findings and highlights therapeutic strategies targeting nucleotide signaling to modulate neutrophil activity in cancer.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Silva et al. (2026) studied this question.

synapsesocial.com/papers/6a168a640c924ddd1bd591abhttps://doi.org/10.1007/s11302-026-10166-2
Ask AI
Helpful
Bookmark
Share
View Full Paper