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慢性压力通过上腺受体β 2/PlexinA1通路促进胃癌的进展

Yanjie Lu¹, Die Cheng², Jiayu Pang²

¹Department of Pathology, Chengde Medical College, Chengde, Hebei Province, China; Cancer Research Laboratory, Chengde Medical College, Chengde, Hebei Province, China.

Cell stress & chaperones

|February 8, 2024

概括

慢性压力通过增加PlexinA1和上腺受体β2的表达来加速胃癌 (GC) 的进展. 阻止上腺素-β2AR/PlexinA1通路可能为GC患者提供新的治疗策略.

科学领域:

在瘤学瘤学.
神经科学是一个神经科学.
分子生物学分子生物学

背景情况:

慢性压力是癌症患者中普遍存在的问题,它会对胃癌 (GC) 的进展和患者的结果产生负面影响.
关联慢性压力与GC进展的精确分子机制仍然不完全理解.

研究的目的:

阐明慢性压力影响GC进展的机制.
在GC中调查慢性压力,PlexinA1表达和患者存活率之间的关联.

主要方法:

对癌症基因组图谱 (TCGA) 和Kaplan-Meier-plotter数据库进行基因表达和生存数据的分析.
用焦虑和抑郁等级评估GC患者的慢性压力.
使用慢性不可预测轻度压力 (CUMS) 诱导小鼠的慢性压力,并评估瘤生长和分子标志物.
药理干预包括化学交感切除和β2上腺素受体对抗.

主要成果:

高PlexinA1水平与GC患者的整体存活率较差相关.
经历慢性压力的GC患者表现出腺受体β2和PlexinA1.1.的表达升高.
在小鼠中,CUMS显著增加了瘤大小,伴随着腺受体β2的上调,PlexinA1,N-cadherin,α-平滑肌动蛋白和Ki67,以及E-cadherin的下调.
经过交感切除术或用β2上腺素受体抗剂治疗后,观察到这些影响的逆转.

结论:

慢性压力显著促进了GC的进展.
上腺素-β2AR/PlexinA1信号通路与压力诱导的GC进展有关.
向上腺素-β2AR/PlexinA1通路为在慢性压力背景下管理GC提供了潜在的治疗策略.

关键词:

上腺体受体β 2 的作用.慢性压力是一种慢性压力.上腺素的使用情况.胃癌胃癌是指胃癌.在PlexinA1A1中使用.

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