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SQSTM1/p62蛋白的核细胞质转位通过稳定EPLIN表达来增强ESCC细胞迁移和入侵
Zou Liu1, Li-Yan Yang2, Jia-Jie Hao1
1State Key Laboratory of Molecular Oncology, Center for Cancer Precision Medicine, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Experimental cell research
|January 7, 2024
概括
细胞质p62通过增加EPLIN稳定性来增强食道癌细胞迁移和入侵. 这种p62的核-细胞质转移可能成为食道状细胞癌 (ESCC) 的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 食道状细胞癌 (ESCC) 是一种具有不良结果的侵袭性癌症.
- 在ESCC进展中p62蛋白细胞局部化的作用尚未完全理解.
- 以前的发现表明p62在ESCC细胞中经历了核细胞质转移.
研究的目的:
- 研究p62独特的细胞定位对ESCC细胞行为的功能影响.
- 阐明p62对ESCC的影响背后的分子机制.
- 确定p62相互作用蛋白及其在ESCC进展中的作用.
主要方法:
- GST拉下测试用于识别p62相互作用蛋白.
- 在ESCC细胞中操纵p62和EPLIN表达水平.
- 细胞迁移和入侵试验的评估.
- 对ESCC组织中EPLIN表达的TCGA和GEO数据库的分析.
主要成果:
- 细胞质p62显著增强ESCC细胞迁移和入侵.
- 核p62对这些细胞功能没有显著影响.
- EPLIN被确定为一种p62相互作用蛋白.
- 减少EPLIN表达抑制ESCC细胞迁移和入侵,效应被EPLIN恢复后的p62敲击所挽救.
- 细胞质p62通过增加其蛋白质稳定性来增强EPLIN表达.
- 在ESCC组织中,EPLIN mRNA的高调显著.
结论:
- 核细胞质转移p62有助于ESCC的攻击性表型.
- 通过EPLIN稳定,p62调节ESCC细胞迁移和入侵.
- p62和EPLIN代表ESCC的潜在分子生物标志物和治疗点.
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