Junzhe He, Yu Zhang, Qian Liu, Biao Yan, Peiwei Chai, Renbing Jia
Future research should further elucidate the mechanistic interplay between pain and cancer, as targeting CRP may offer novel therapeutic opportunities for anti-cancer treatment.
BACKGROUND: Cancer-related pain (CRP), with a high prevalence and prognostic value in malignancies, is not only a passive phenomenon but rather engages in a bidirectional crosstalk with cancer progression.
MAIN TOPICS: This review focuses on the intricate reciprocal relationship between CRP and cancer progression, delineating how advanced cancers promote CRP directly through tissue destruction, invasion and inflammation, or indirectly via inflammatory, neural, stromal and metabolic components within the tumour microenvironment. However, controversies remain in the field, such as the ambiguous role of sensory neurons in cancer progression and the potential pro-tumorigenic risk of opioids. Notably, CRP regulates cancer progression through local pain-associated mediators (e.g., CGRP, SP), the pain-stress axis, central nuclei-mediated peripheral immune modulation, sensory-sympathetic/vagal circuits and direct effects on tumour biology.
CONCLUSION: Future research should further elucidate the mechanistic interplay between pain and cancer, as targeting CRP may offer novel therapeutic opportunities for anti-cancer treatment.
HIGHLIGHTS: CRP and tumour progression engage in a dynamic, bidirectional circuit mediated by multiple mechanisms in neuroimmunology and cancer neuroscience. Analgesic interventions may affect tumour progression, while anticancer therapies can influence pain. Targeting pain in cancer may have promising therapeutic value in cancer progression.