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通过依赖激酶激活AKT,CASK促进前列腺癌的进展
Varsha Rathore1, Ching-Yuan Cheng2, Shao-Peng Chen2
1Chemical Biology and Molecular Biophysics, Taiwan International Graduate Program, Academia Sinica, Taipei 115201, Taiwan; Institute of Biotechnology, College of Life Sciences and Medicine, National Tsing Hua University, Hsinchu 300044, Taiwan; Department of Pharmacology, College of Medicine, National Taiwan University, Taipei 100233, Taiwan.
概括
/卡尔莫杜林依赖的血清蛋白激酶 (CASK) 促进前列腺癌 (PCa) 的进展. 正如在小鼠模型中证实的那样,CASK通过激活AKT来增强PCa细胞迁移和入侵,独立于TGF-β信号传递.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 细胞信号传递 细胞信号传递
背景情况:
- 在前列腺癌 (PCa) 进展中,/卡尔莫杜林依赖的血清蛋白激酶 (CASK) 的作用以前是未知的.
- 了解CASK的功能对于开发针对PCa的新治疗策略至关重要.
研究的目的:
- 调查CASK在前列腺癌进展中的作用,特别是细胞迁移和侵入.
- 阐明CASK影响PCa细胞行为的信号通路.
主要方法:
- 在PCa组织中分析了CASK表达水平.
- 在PCa细胞系 (PC3和LNCaP) 中进行了透视病毒介导的CASK沉默.
- 评估了细胞迁移,入侵和蛋白质化 (Smad2/3,ERK,AKT). 激酶抑制剂和共免疫沉降被用于探索CASK-AKT相互作用. 采用异种移植小鼠模型来评估瘤发生效应.
主要成果:
- 在PCa组织中,CASK被上调.
- CASK静音降低了PCa细胞的迁移和入侵,独立于TGF-β刺激.
- CASK静音降低了TGF-β诱导的AKT酸化,但没有影响Smad2/3或ERK酸化.
- CASK与AKT相互作用,并在S473.3增强其酸化.
- 抑制CASK,AKT或CaMKII可以减少细胞入侵和迁移.
- 在体内,CASK促进瘤生长.
结论:
- CASK作为前列腺癌进展的促进剂.
- CASK通过激酶依赖的AKT信号的激活来增强PCa细胞迁移和入侵.
- 这种机制独立于TGF-β诱导的Smad2/3和ERK通路.
- 在前列腺癌治疗中,CASK是潜在的治疗点.
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