LEPR/FOS/JUNB信号通路有助于慢性抑制压力诱导的瘤增殖
Jian Zhu1, Qing Liu2, Shuang Nie2
1School of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, 333 Longteng Road, Shanghai, 201620, China; Department of Naval Nutrition and Food Hygiene, Naval Medical University, Shanghai, 200433, China.
Biochemical and biophysical research communications
|May 18, 2024
概括
慢性压力通过激活北上腺素 (NE) - 莱普丁受体 (LEPR) 途径来加速瘤的生长. 这一途径涉及FOS和JUNB,促进癌细胞存活和增殖,突出了压力诱导瘤发展的新机制.
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:
- 心理社会压力与瘤发展有关.
- 慢性压力会增加上腺素 (NE) 和瘦素受体 (LEPR) 的表达,促进瘤入侵,转移和扩散.
- 慢性压力诱导的瘤增殖的确切机制尚未完全理解.
研究的目的:
- 为了研究慢性压力对瘤增殖的影响.
- 为了阐明参与慢性压力诱导瘤生长的分子途径.
主要方法:
- 建立具有慢性抑制应激 (CRS) 的皮下瘤模型.
- 对来自肝癌患者的转录学数据的分析.
- 在体外验证使用细胞培养和基因沉默的目标途径.
主要成果:
- 与对照组相比,CRS显著增加了瘤大小.
- 在瘤组织中,CRS增加了LEPR,FOS和JUNB的mRNA水平.
- 上腺素 (NE) 在体外增强了癌细胞存活率和LEPR-FOS-JUNB表达;LEPR沉默降低了细胞活力.
结论:
- 慢性克制压力 (CRS) 通过NE激活LEPR-FOS-JUNB信号通路,加剧瘤的发展.
- 这项研究为了解慢性压力条件下的瘤进展提供了机制基础.
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