Epigenetic mechanisms of bone cancer pain

The management and treatment of bone cancer pain (BCP) remain significant clinical challenges, imposing substantial economic burdens on patients and society. Extensive research has demonstrated that BCP induces changes in the gene expression of peripheral sensory nerves and neurons, which play crucial roles in the onset and maintenance of BCP. However, our understanding of the epigenetic mechanisms of BCP underlying the transcriptional regulation of pro-nociceptive (such as inflammatory factors and the transient receptor potential family) and anti-nociceptive (such as potassium channels and opioid receptors) genes remains limited. This article reviews the epigenetic regulatory mechanisms in BCP, analyzing the roles of histone modifications, DNA methylation, and noncoding RNAs (ncRNAs) in the expression of pro-nociceptive and anti-nociceptive genes. Finally, we provide a comprehensive view of the functional mechanisms of epigenetic regulation in BCP and explore the potential of these epigenetic molecules as therapeutic targets for BCP. •The mechanisms by which epigenetics play a role in bone cancer pain were comprehensively and clearly elucidated.•Key molecules involved in bone cancer pain, as well as potential targets and promising therapeutic approaches, were summarized.•The challenges and future directions in the field of epigenetic regulation of bone cancer pain were summarized and discussed.