Fig. 2

The interplay between sleep–wake cycles and cancer. a sleep–wake cycles regulate the immune system. During normal sleep–wake cycles, SWS sustains the function of immune system by maintaining the balance of T-helper1 (Th1) and T-helper2 (Th2) cell-derived cytokines (Th1 cytokines: IL-2, IFNγ, and IL-12; Th2 cytokines: IL-4 and IL-10), which benefit the antigen presenting process. b sleep–wake cycles regulate the inflammatory response. Disturbance of sleep continuity (sleep time and efficiency) and architecture (SWS and REM sleep) may lead to body inflammatory response, including abnormal systemic inflammation, cellular inflammation and inflammation transcriptional activity, which are associated with development of chronic inflammation related disease, such as cancers. c Sleep–wake cycles and endocrine. Endocrine factors, including growth hormone, prolactin, thyroid hormone, cortisol, gonadal steroids, insulin, and so on, have been identified to be secreted during certain time periods. Disruption of sleep–wake cycles may break these balances and influence their secretions. d Sleep–wake cycles regulate DNA damage and repair. On the one hand, sleep disruption can reduce the levels of melatonin, an important antioxidant, which may lead to increased oxidative DNA damage. On the other hand, sleep deprivation downregulates the expression of several genes involved in DNA repair, such as ERCC6, PARP1, and RAD50, which may ultimately promote tumorigenesis. e, Feedback from cancer to sleep–wake cycles. IL-1β in the brain can regulate REM and NREM sleep by modulating various molecules and neurotransmitters, including COX-2, GABA, and nitric oxide (NO), while IL-6 enhances SWS and decreases REM sleep. SWS: slow-wave sleep; REM: rapid eyes movement; TSH: thyroid-stimulating hormone; PRL: prolactin; RAAS: renin–angiotensin–aldosterone systems; COX-2: cyclooxygenase-2.