Advances in cancer pain from bone metastasis

Abstract

With the technological advances in cancer diagnosis and treatment, the survival rates for patients with cancer are prolonged. The issue of figuring out how to improve the life quality of patients with cancer has become increasingly prominent. Pain, especially bone pain, is the most common symptom in malignancy patients, which seriously affects the life quality of patients with cancer. The research of cancer pain has a breakthrough due to the development of the animal models of cancer pain in recent years, such as the animal models of mouse femur, humerus, calcaneus, and rat tibia. The establishment of several kinds of animal models related to cancer pain provides a new platform in vivo to investigate the molecular mechanisms of cancer pain. In this review, we focus on the advances of cancer pain from bone metastasis, the mechanisms involved in cancer pain, and the drug treatment of cancer pain in the animal models.

Keywords: animal models of cancer pain; cancer pain from bone metastasis; drug treatment; molecular mechanisms.

Figure 1

Mechanism of bone cancer pain. Notes: In the process of bone cancer pain, cancer cells secrete diverse cell factors to promote proliferation and stimulate osteoclastic bone resorption via activation of receptor activator of the nuclear factor-kB (RANKL)/RANK pathway in osteoblasts and osteoclasts. Bone-resorbing osteoclasts secrete protons to degrade bone minerals and form a highly acidic microenvironment. Then, the acidic microenvironment directly excites sensory neurons innervating bone via activation of the acid-sensing nociceptors, TRPV1 (transient receptor potential vanilloid 1) and ASIC3 (acid-sensing ion channel 3), transducing noxious signals via DRG (primary afferent neuron), and spinal cord (secondary afferent neuron) and evokes bone pain in brain. Abbreviation: DRG, dorsal root ganglia.