非典型的卡德林FAT1通过抑制质母细胞瘤的自细胞死亡在低氧或营养压力下促进瘤发生
在PubMed上查看摘要
概括
此摘要是机器生成的。在质母细胞瘤中,FAT1蛋白抑制了自性细胞死亡,促进了癌症的生长. 抑制FAT1可以通过重新激活这种细胞死亡途径来增强癌症治疗.
科学领域
- 癌症学
- 细胞生物学
- 分子生物学
背景情况
- 自在癌症中起着双重作用, 促进细胞存活或死亡.
- 非典型的cadherin FAT1具有取决于环境的致癌或瘤抑制功能.
- 在质母细胞瘤中,FAT1是致癌的,在质母细胞瘤中,自是不受调节的.
研究的目的
- 研究FAT1在质母细胞瘤中调节自的作用.
- 确定FAT1调节的自对质母细胞瘤生长和进展的影响.
主要方法
- 在质母细胞瘤,肝细胞癌和胰腺癌细胞系中使用CRISPR- Cas9产生FAT1淘汰.
- 评估细胞活力,生长和自标志物 (qPCR,西部斑块,ICC,IHC,TEM,p62/SQSTM1,LC3点).
- 评估了自流量,并分析了体外移植和人类质母细胞瘤的数据.
主要成果
- 减少了质母细胞细胞存活率和殖民地形成,诱导了自性细胞死亡.
- 增加了自细胞和自细胞流量,并降低了mTOR信号.
- 人类瘤呈现反向的FAT1/ LC3B相关性,高FAT1与低生存率相关.
结论
- 通过抑制自细胞死亡,FAT1促进质母细胞瘤和其他癌症.
- 对于具有高FAT1表达和致癌作用的癌症,FAT1可能是治疗点或辅助剂.
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