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芦苔凝胶葡甘露聚糖通过线粒体损伤驱动的 PINK1/Parkin 线粒体自噬通路诱导结肠癌细胞死亡。

Aloe gel glucomannan induced colon cancer cell death via mitochondrial damage-driven PINK1/Parkin mitophagy pathway.

机构信息

State Key Laboratory of Food Science and Technology, China-Canada Joint Laboratory of Food Science and Technology (Nanchang), Key Laboratory of Bioactive Polysaccharides of Jiangxi Province, Nanchang University, China.

State Key Laboratory of Food Science and Technology, China-Canada Joint Laboratory of Food Science and Technology (Nanchang), Key Laboratory of Bioactive Polysaccharides of Jiangxi Province, Nanchang University, China.

出版信息

Carbohydr Polym. 2022 Nov 1;295:119841. doi: 10.1016/j.carbpol.2022.119841. Epub 2022 Jul 8.

Abstract

Mitophagy can selectively remove damaged mitochondria, which is critical in regulating mitochondrial homeostasis in diseases, such as cancer. Herein, we found that Aloe gel glucomannan (AGP) significantly inhibited the proliferation of colon cancer cells. RNA-seq analysis revealed that AGP upregulated autophagy, lysosome and mitochondrial fission signal pathways in colon cancer cell line CT26. Notably, AGP induced the accumulation of impaired and reactive oxygen species (ROS)-generating mitochondria, which triggered excessive mitophagy. Interestingly, the mitophagy activator enhanced AGP-induced mitophagy and cytotoxicity, whereas the mitophagy inhibitor reversed the influence of AGP. Furthermore, activation of PINK1/Parkin mitophagy pathway and transcription factor EB (TFEB) signaling was dependent on ROS overproduction. Taken together, these results indicated that AGP induced cytotoxic mitophagy through ROS-related PINK1/Parkin pathway and TFEB activation in CT26 cells. The research would provide theoretical basis for the development of AGP as a promising anticancer agent.

摘要

自噬可以选择性地去除受损的线粒体,这对于调节癌症等疾病中线粒体的动态平衡至关重要。在此,我们发现,库拉索芦荟凝胶葡甘聚糖(AGP)可显著抑制结肠癌细胞的增殖。RNA-seq 分析显示,AGP 在上皮样癌细胞系 CT26 中上调了自噬、溶酶体和线粒体分裂信号通路。值得注意的是,AGP 诱导了受损和产生活性氧物质(ROS)的线粒体的积累,从而引发了过度的自噬。有趣的是,自噬激活剂增强了 AGP 诱导的自噬和细胞毒性,而自噬抑制剂则逆转了 AGP 的影响。此外,PINK1/Parkin 自噬途径和转录因子 EB(TFEB)信号的激活依赖于 ROS 的过度产生。综上所述,这些结果表明,AGP 通过 ROS 相关的 PINK1/Parkin 途径和 TFEB 的激活诱导 CT26 细胞发生细胞毒性自噬。这项研究为开发 AGP 作为一种有前途的抗癌药物提供了理论基础。

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