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Poor sleep drives cancer growth by decreasing a type of immune cell that eliminates tumors.
Scientists have long known that people who don’t get enough sleep are at greater risk of developing cancer. Once a person develops cancer, how long and how well they sleep can influence their disease outcome. A 2014 study implicated tumor-associated macrophages and toll-like receptor (TLR)- 4 as the primary drivers of unfavorable cancer outcomes in the setting of poor sleep.
Tumor-associated macrophages are white blood cells that play important roles in cancer progression. M1 macrophages, which have a proinflammatory phenotype, can eliminate cancer cells. M2 macrophages, which have an anti-inflammatory phenotype, suppress immune activity and promote blood vessel growth – a critical aspect of tumor survival.
TLR-4 is a receptor protein found on the surface of immune and other cells. TLR-4 activates transcription factors that promote the expression of pro-inflammatory cytokines. While this inflammatory response is necessary for immunity against bacterial infection, chronic activation of the TLR-4 pathway can accelerate aging and increase the risk for many diseases, including cancer.
The investigators interrupted the sleep of normal mice and mice that lacked TLR-4, mimicking the effects of several sleep disorders. After the mice developed cancer, the investigators noted characteristics of the animals' tumors, including size, invasiveness, and the type and number of tumor-associated macrophages.
They found that the mice that experience interrupted sleep had larger, more invasive tumors and larger numbers of tumor-associated macrophages than the mice that had uninterrupted sleep. However, these effects were not observed in the mice that lacked TLR4.
These findings suggest that poor, fragmented sleep promotes tumor growth and invasiveness via activation of TLR4 pathways and subsequent recruitment of tumor-associated macrophages. Learn more about the varied roles TLR4 plays in human health in our overview article.
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