Faculty Proceedings, Presentations, Speeches and Lectures

Sleep Deprivation Results in Increased Expression of Cancer-Related MiRNAs in Humans

Event Name/Location

31st Annual Meeting of the Associated Professional Sleep Societies LLC (APSS)

Event Location / Date(s)

Boston, MA

Presentation Date

6-3-2017

Document Type

Poster

Description

Introduction: A large and growing body of evidence shows that sleep loss has profound deleterious effects on health and has been specifically linked to the development of several cancers. Despite this obvious health cost, there is almost no current understanding of how sleep loss increases the risk for tumor development. The purpose of the present study was to identify epigenetic mechanisms through which total sleep deprivation (TSD) altered expression of known cancer-related genes (suppressors and promoters). To that end, we tested the effects of TSD on the expression of miRNAs that are associated with tumor development.

Methods: Twenty-three participants (14 males, mean age = 20) underwent actigraphy-verified TSD for 24 hours in a controlled environment. miRNA preparations were extracted from participants’ plasma and processed for cDNA synthesis. The resulting cDNA pools were used as templates in qPCR reactions in an effort to estimate differential miRNA expression.

Results: Results indicated that sleep deprivation caused significant differential expression of several specific miRNA tumor-related genes, including miR-15a, miR-96, and miR-296-5p. Accordingly, further tests were focused on these two miRNA species on a subset of participants. Results showed that, there was a significant upregulation of miR-15a (p < 0.05), miR-96 (p < 0.05), and miR-22 (p < 0.05), but not miR-296-5p (p=0.12).

Conclusion: Overall, these findings show how even short-term sleep loss can alter cancer-associated pathways. Increased expression of miR-15a and miR-22 have known tumor suppression properties. It is possible that miR-15a and miR-22 exert protective effects in response the TSD-induced disruption to homeostasis. Although miR-96 is a known oncogene, it is also part a complex clock gene signaling pathway with diurnal expression. Accordingly, TSD potentially disrupts the normal diurnal expression pattern miR-96. We are currently following up on these results in a study of people who regularly experience sleep loss (i.e. chronic sleep restriction).

Support (If Any): This work is supported by the Department of Education. Number P120A1400.

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