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在人类乳腺癌细胞中通过ATF6α的异位表达诱导的细胞衰老的转录组分析
Ju Won Kim1, So-Hyun Bae2, Yesol Moon1,3
1Department of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, South Korea.
PloS one
|October 28, 2024
概括
细胞内膜网膜 (ER) 压力通过ATF6α通路触发乳腺癌细胞中的细胞衰老. 像MAP2K1/2和GPAT4这样的关键调节器驱动这个过程,影响细胞活力和死亡.
科学领域:
- 分子生物学分子生物学
- 癌症研究 癌症研究
- 细胞衰老 细胞衰老
背景情况:
- 细胞衰老表现出不同的转录组形状,受细胞类型,压力因素和衰老阶段的影响.
- 研究特定的细胞类型和压力因素对于理解衰老至关重要.
- 展开蛋白质反应 (UPR) 的ATF6α分支在内质网膜 (ER) 压力诱导的衰老中发挥作用.
研究的目的:
- 阐明ER在MCF-7乳腺癌细胞中因应激诱导的细胞衰老的分子机制.
- 专注于ATF6α通路在这个过程中的作用.
- 在ATF6α异位表达后进行转录组分析.
主要方法:
- 在ATF6α表达后6小时和9小时进行MCF-7细胞的转录组测序.
- 使用功能注释,途径分析和网络分析分析差异表达基因 (DEGs) 的分析.
- 通过RNA干扰和与衰老相关的β-galactosidase染色来验证已识别的上游调节剂和基因.
主要成果:
- 在6小时和9小时,ATF6α表达分别导致了12和79个DEG.
- 分析表明UPR和ER应激通路的参与.
- 与细胞静止和细胞死亡相关的关键调节剂 (MAP2K1/2,GPAT4,PDGF-BB) 和标 (DDIT3,PPPP1R15A,IL6) 被确定并验证.
结论:
- 在MCF-7细胞中,MAP2K1/2/GPAT4-DDIT3通路对于ATF6α诱导的细胞衰老至关重要.
- 这项研究增强了对乳腺癌中ER压力诱导衰老的早期分子事件的理解.
- 为进一步研究细胞类型和压力特异性衰老反应提供了基础.
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