| Literature DB >> 25949873 |
Jiamao Zheng1, Isaac Almendros1, Yang Wang1, Shelley X Zhang1, Alba Carreras1, Zhuanhong Qiao1, David Gozal1.
Abstract
The molecular mechanisms underlying how sleep fragmentation (SF) influences cancer growth and progression remain largely elusive. Here, we present evidence that SF reduced ROS production by downregulating gp91phox expression and activity in TC1 cell tumor associated macrophages (TAMs), while genetic ablation of phagocytic Nox2 activity increased tumor cell proliferation, motility, invasion, and extravasation in vitro. Importantly, the in vivo studies using immunocompetent syngeneic murine tumor models suggested that Nox2 deficiency mimics SF-induced TAMs infiltration and subsequent tumor growth and invasion. Taken together, these studies reveal that perturbed sleep could adversely affect innate immunity within the tumor by altering Nox2 expression and activity, and indicate that selective potentiation of Nox2 activity may present a novel therapeutic strategy in the treatment of cancer.Entities:
Keywords: ANOVA, Analysis of variance; FBS, fetal bovine serum; HEPES, 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid; MFI, median fluorescence intensities; NADPH oxidase; Nox2, NADPH Oxidase Type 2; PMA, phorbol 12-myristate 13-acetate; ROS, reactive oxygen species; SE, standard error; SF, sleep fragmentation; TAMs, tumor associated macrophages; TLR-4, toll like receptor 4; WT, wild type; cancer; reactive oxygen species; rpm, revolutions per minute; sleep apnea; tumor associated macrophage
Year: 2015 PMID： 25949873 PMCID： PMC4404846 DOI： 10.4161/2162402X.2014.976057
Source DB: PubMed Journal: Oncoimmunology ISSN： 2162-4011 Impact factor: 8.110