PAR2 on oral cancer cells and nociceptors contributes to oral cancer pain that can be relieved by nanoparticle-encapsulated AZ3451

Bhansali D
October 9, 2024
Biomaterials
https://pubmed.ncbi.nlm.nih.gov/39418848/

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/39418848/

Research summary

This study investigates the role of protease-activated receptor 2 (PAR2) in oral cancer pain. Using a nociceptive sensory neuron-specific conditional Knockout (CKO) mouse model, the researchers demonstrated that deletion of F2rl1 (encoding PAR2) in nociceptors partially alleviated mechanical allodynia associated with oral cancer. Additionally, nanoparticle-encapsulated AZ3451, a PAR2 antagonist, effectively reversed PAR2 activation and provided greater antinociceptive efficacy compared to the free drug.

Key outcome of the study

PAR2 expressed on both oral cancer cells and nociceptors contributes to cancer-induced mechanical allodynia. Targeted deletion of PAR2 in nociceptors reduces pain, and nanoparticle-mediated delivery of a PAR2 antagonist offers enhanced pain relief.

Mouse model

Nociceptive sensory neuron-specific conditional Knockout (CKO) mouse model, generated by crossing F2rl1^flox/flox mice with Nav1.8-Cre transgenic mice to delete PAR2 specifically in nociceptors.

TARGET:
F2rl1
PAR2, Protease-activated receptor 2

Keywords

Oral cancer pain, PAR2, Nociceptors, Nanoparticle drug delivery, Cancer-induced allodynia

Technical specifications

Conditional Knockout model, Nav1.8-Cre driver, PAR2 antagonist, Nanoparticle encapsulation

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