癌症中的压力关系:乳腺肿瘤的肾上腺素能燃料

IF 2.5 Q2 PHYSIOLOGY Current Opinion in Physiology Pub Date : 2023-10-06 DOI:10.1016/j.cophys.2023.100720
Angela Albitre , Clara Reglero , Teresa González-Muñoz , Petronila Penela
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引用次数: 0

摘要

癌症的进展涉及肿瘤细胞与周围微环境之间复杂的相互作用。慢性社会心理压力和交感神经系统激活导致儿茶酚胺释放异常,直接或间接影响肿瘤细胞并促进癌症的发生。然而,介导这些影响的肾上腺素能受体(AR)也可能传达与运动相关的有益变化。流行病学研究显示压力、AR抑制剂和乳腺癌(BC)转移进展之间存在相互矛盾的关联。肾上腺素能交感应激触发持续炎症和缺氧相关的信号通路,改变免疫细胞群的功能和分布,重塑血管,导致免疫抑制和转移前部位形成。激活的AR启动酪氨酸激酶受体和趋化因子受体的反馈回路,影响干相关转录因子、促炎介质、血管生成因子和能量代谢调节因子,促进肿瘤生长和侵袭。了解激动和拮抗AR配体的分子机制以及与其他信号通路的串扰对于开发针对肾上腺素能驱动的BC进展的有效疗法至关重要。
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The stress connection in cancer: the adrenergic fuelling of breast tumors

Cancer progression involves complex interactions between tumor cells and the surrounding microenvironment. Chronic psychosocial stress and sympathetic nervous system activation lead to abnormal catecholamine release, impacting tumor cells directly and indirectly and fuelling cancer-promoting effects. However, the same adrenergic Receptor (AR) that mediate these effects could also convey exercise-related beneficial changes. Epidemiological studies show conflicting associations between stress, AR inhibitors, and breast cancer (BC) metastatic progression. Adrenergic sympathetic stress triggers sustained inflammatory and hypoxic-related signaling pathways, alters function and distribution of immune cell populations, and remodels blood vessels, leading to immunosuppression and premetastatic site formation. Activated AR initiate feedback loops with tyrosine kinase receptors and chemokine receptors, affecting stem-related transcription factors, pro-inflammatory mediators, angiogenic factors, and energy metabolism regulators, promoting tumor growth and invasion. Understanding molecular mechanisms of agonistic and antagonistic AR ligands and crosstalk with other signaling pathways is crucial for developing effective therapies targeting adrenergic-driven BC progression.

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来源期刊
Current Opinion in Physiology
Current Opinion in Physiology Medicine-Physiology (medical)
CiteScore
5.80
自引率
0.00%
发文量
52
期刊最新文献
Publisher's Note Editorial Board Editorial Board Publisher's Note Adrenergic modulation of neutrophil and macrophage functions: pathophysiological cues
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