Regulation of cancer progression by β-endorphin neuron.
Regulation of cancer progression by β-endorphin neuron.
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DOI：
10.1158/0008-5472.can-11-3292
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发表时间：
2012-02-15
期刊：
影响因子：
11.2
通讯作者：
Boyadjieva N
中科院分区：
文献类型：
--
作者：
Sarkar DK;Murugan S;Zhang C;Boyadjieva N
越来越清楚的是，压力性生活事件可以通过调节神经，内分泌和免疫系统来影响癌症的生长和转移。这篇综述的目的是简要描述应激可能增强致癌作用的过程，以及如何减少身体应激可以防止癌症的生长和进展。阿片肽β-内啡肽（BEP）在使应激轴达到稳态中起着关键作用。我们最近发现，通过BEP神经元移植增强下丘脑中的内源性BEP水平抑制应激反应，促进免疫功能，并降低前列腺癌和乳腺癌大鼠模型的癌症发病率。BEP的癌症预防作用是通过抑制交感神经元功能介导的，这导致外周自然杀伤（NK）细胞和巨噬细胞活性增加、抗炎细胞因子水平升高和炎性细胞因子水平降低。BEP对肿瘤进展的抑制还涉及肿瘤微环境的改变，这可能是由于抑制了已知改变DNA修复、细胞-基质附着、血管生成过程和上皮-间充质转化的儿茶酚胺和炎性细胞因子的产生。因此，BEP细胞疗法可能在癌症预防中提供一些治疗价值。
It is becoming increasingly clear that stressful life events can impact cancer growth and metastasis by modulating nervous, endocrine and immune systems. The purpose of this review is to briefly describe the process by which stress may potentiate carcinogenesis and how reducing body stress may prevent cancer growth and progression. The opioid peptide beta-endorphin (BEP) plays a critical role in brining the stress axis to a state of homeostasis. We have recently shown that enhancement of endogenous levels of BEP in the hypothalamus via BEP neuron transplantation suppresses stress response, promotes immune function and reduces the incidence of cancer in rat models of prostate and breast cancers. The cancer preventive effect of BEP is mediated through the suppression of sympathetic neuronal function that results in an increased peripheral natural killer (NK) cell and macrophage activities, elevated levels of anti-inflammatory cytokines and reduced levels of inflammatory cytokines. BEP inhibition of tumor progression also involves alteration in the tumor microenvironment, possibly due to suppression of catecholamine and inflammatory cytokines production that are known to alter DNA repair, cell-matrix attachments, angiogenic process and epithelial-mesenchymal transition. Thus, BEP cell therapy may offer some therapeutic value in cancer prevention.