P2X2/3 receptors as a potential target for cancer pain treatment.

In the process of tumor growth and metastasis, which can invade nerve tissue, sensitize peripheral receptors, enhance sensory information transmission and induce pain. Bone cancer pain is the most common type of cancer pain, caused by primary bone tumors or other types of cancer metastasis, destruction and dissolution of bone tissue, leading to pain generation. The pathological mechanism of cancer pain is complex and its treatment is a thorny problem at present. P2X2/3 receptors are mainly expressed in nociceptive sensory neurons. ATP released by cells is involved in nociceptive and pain signal transduction by activating or sensitizing P2X2/3 receptors. ATP-activated P2X2/3 receptors can produce rapid or continuous desensitized transient current, resulting in abnormal activity of sensory neurons and enhanced synaptic plasticity, sensitizing the central nervous system and leading to pain. A few studies have shown that P2X2/3 receptors may play a regulatory role in tumor progression, which also strengthens the functional role of P2X2/3 receptors in cancer pain. However, the use of P2X2/3 receptors antagonists (such as A31749 and AF-353) can antagonize the activation of P2X2/3 receptors and have pharmacological effects on pain relief. Therefore, in this article, we discuss the potential relationship between P2X2/3 receptors and cancer pain and its potential pharmacological target for the treatment of cancer pain.