Inhibiting STAT3 in a murine model of human breast cancer-induced bone pain delays the onset of nociception

Aggressive breast cancer subtypes utilize system x_c^-, a membrane antiporter, to import cystine for glutathione synthesis and maintenance of redox homeostasis, in turn releasing glutamate as a metabolic pro-nociceptive by-product. Metastatic breast cancers establish themselves at distal sites including bone, where changes in extracellular glutamate levels contribute to cancer-induced bone pain. We previously established that stearically blocking …