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肝细胞生长因子促进黑色素瘤转移通过泛素特异性化酶22介导整合素上调调节
Qiong Gao1, Na Li2, Yujie Pan2
1Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Dalian Medical University, Dalian, 116044, China; Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Cancer letters
|September 2, 2024
概括
乌比基特异性酶22 (USP22) 对于肝细胞生长因子 (HGF) 诱导的黑色素瘤转移至关重要. USP22二基化Sp1,增强整合蛋白表达并促进瘤的扩散.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 肝细胞生长因子 (HGF) 通过调节整合素,促进瘤细胞迁移,入侵和转移.
- 连接HGF与整合素介导瘤发生的精确分子机制仍然不完全理解.
研究的目的:
- 研究基因特异性酶22 (USP22) 在高基因诱导的黑色素瘤转移中的作用.
- 阐明USP22调节整合素表达并促进瘤进展的分子机制.
主要方法:
- 利用HGF治疗,CRISPR介导的基因删除和西式涂抹来评估蛋白质表达和无处不在.
- 进行TCGA数据库分析以确定USP22和HGF在各种癌症中的下游目标.
- 在人类黑色素瘤组织上进行免疫组织化学,以相关联USP22,Sp1和整蛋白αv表达.
主要成果:
- 在黑色素瘤细胞中,HGF治疗显著增加了USP22和整蛋白 (ITGAV,ITGB3,ITGA1) 表达.
- 通过CRISPR删除USP22消除了HGF诱导的整蛋白表达.
- USP22二基化Sp1,防止其蛋白质体降解,从而增加ITGAV,ITGB3和ITGA1.1的转录.
- 在人类黑色素瘤组织中观察到USP22,Sp1和integrin αv之间的正相关性.
结论:
- USP22对于HGF诱导的黑色素瘤转移是必不可少的.
- USP22作为Sp1的二维基因酶起作用,Sp1是参与黑色素瘤进展的整合素的关键转录因子.
- USP22代表了抑制黑色素瘤转移的潜在治疗标.
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