作者: Qiang Lin , Feifei Wang , Rong Yang , Xinmin Zheng , Huibao Gao
DOI: 10.1371/JOURNAL.PONE.0061435
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摘要: Stress alters immunological and neuroendocrinological functions. An increasing number of studies indicate that chronic stress can accelerate tumor growth, but its role in colorectal carcinoma (CRC) progression is not well understood. The aim this study to investigate the effects restraint (CRS) on CRC cell growth nude mice possible underlying mechanisms. In study, we showed CRS increased levels plasma catecholamines including epinephrine (E) norepinephrine (NE), stimulated cell-derived tumors vivo. Treatment with adrenoceptor (AR) antagonists phentolamine (PHE, α-AR antagonist) propranolol (PRO, β-AR significantly inhibited CRS-enhanced mice. addition, hormones E NE remarkably enhanced proliferation viability culture, as These were antagonized by AR PHE PRO, indicating hormone-induced dependent. We also observed atenolol (ATE, β1- ICI 118,551 (ICI, β2- decreased phosphorylation extracellular signal-regulated kinases-1/2 (ERK1/2) vitro ERK1/2 inhibitor U0126 blocked function hormone, suggesting involvement tumor-promoting effect CRS. conclude promotes xenograft stimulating through signaling-dependent activation ERK1/2.