在KDEL受体和EGF受体之间的交叉声调解细胞增殖和迁移通过STAT3信号传递
Jie Jia1, Lianhui Zhu1, Xihua Yue1
1School of Life Science and Technology, ShanghaiTech University, Pudong, Shanghai, China.
Cell communication and signaling : CCS
|February 20, 2024
概括
分泌的内等质网膜 (ER) 陪伴者促进癌症的生长. KDEL受体 (KDELR) 作为细胞表面受体,与EGF受体 (EGFR) 相互作用,激活STAT3信号,驱动瘤细胞的增殖和迁移.
科学领域:
- 细胞生物学 细胞生物学
- 癌症研究 癌症研究
- 分子瘤学分子瘤学
背景情况:
- 癌细胞创造了一个敌对的微环境,压力内质网膜 (ER).
- 这种压力刺激ER伴侣表达和分泌,促进瘤的进展.
- 精确的分子机制连接分泌的伴侣与瘤发生并未完全理解.
研究的目的:
- 阐明分泌ER陪伴剂促进癌细胞增殖和迁移的分子机制.
- 为了确定细胞表面受体和参与调解这些效应的信号通路.
主要方法:
- 基于近距离的质谱法.
- 分裂金星成像成像
- 膜酵母两种混合测试试验
主要成果:
- 随伴ER的KDEL图案对于调解细胞增殖和迁移至关重要.
- 皮表皮生长因子受体 (EGFR) 作为细胞表面KDEL受体 (KDELR) 的共同受体.
- 在联体结合时,KDELR与EGFR相互作用,导致EGFR的C端氨酸酸化和STAT3激活,从而驱动细胞生长和迁移.
结论:
- KDELR作为分泌的ER伴侣的细胞表面受体起作用.
- 分泌的ER伴侣激活EGFR-STAT3信号通路,促进癌症的进展.
- 针对KDELR-EGFR-STAT3轴可能为癌症治疗提供治疗策略.
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