Sleep deprivation may accelerate prostate cancer progression by activating the CXCL13/CXCR5/JNK signaling axis, as demonstrated through clinical questionnaire data linking worse sleep quality to higher Gleason scores and in vivo mouse models showing accelerated tumor growth.
Worse sleep quality in prostate cancer patients correlates with higher Gleason scores.
Sleep deprivation accelerated tumor growth in a mouse model of prostate cancer.
Transcriptome sequencing revealed that inflammation-related pathways were activated in the sleep deprivation mouse model.
CXCL13 was identified as a key mediator of sleep deprivation-induced prostate cancer progression.
Inhibition of CXCR5, the receptor for CXCL13, reduced the tumor-promoting effects of sleep deprivation.
CXCL13 enhanced prostate cancer cell proliferation via activation of the JNK signaling pathway.
The authors conclude that sleep deprivation may accelerate prostate cancer progression through the CXCL13/CXCR5/JNK signaling axis, providing a potential therapeutic direction.
This research suggests that poor sleep may not just be a side effect of having prostate cancer, but may actually help the cancer grow faster. The study found that prostate cancer patients who reported worse sleep quality also tended to have higher Gleason scores, which is a measure of how aggressive or advanced their cancer is. To understand why this might happen, the researchers also studied mice with prostate cancer that were deprived of sleep, and found that these mice had faster tumor growth compared to mice that slept normally. To figure out the biological reason behind this connection, the researchers analyzed gene activity in the sleep-deprived mice and found that pathways related to inflammation were turned on. They pinpointed a specific molecule called CXCL13 — a type of signaling protein involved in immune responses — as a key driver of this effect. CXCL13 works by binding to a receptor called CXCR5 on cancer cells, which then activates a chain of molecular signals (through a pathway called JNK) that makes cancer cells multiply faster. When the researchers blocked CXCR5, the tumor-promoting effects were reduced, suggesting this pathway is functionally important. This research suggests that disrupted sleep could create biological conditions that make prostate cancer more aggressive, and that the CXCL13/CXCR5/JNK signaling chain may be one mechanism through which this happens. The findings are described as preliminary, but they point toward a potential avenue for future treatments that might target this pathway. More research would be needed to confirm these findings in humans and determine whether interventions targeting sleep or this molecular pathway could affect cancer outcomes.
Zhang J, Yang L, He J, Li W, Wang H, Liang C. (2026). The role of sleep deprivation in prostate cancer and a preliminary exploration of its mechanisms.. Pathology, research and practice. https://doi.org/10.1016/j.prp.2026.156379