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.
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.
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.
Oral cancer pain, PAR2, Nociceptors, Nanoparticle drug delivery, Cancer-induced allodynia
Conditional Knockout model, Nav1.8-Cre driver, PAR2 antagonist, Nanoparticle encapsulation
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