研究动态
Articles below are published ahead of final publication in an issue. Please cite articles in the following format: authors, (year), title, journal, DOI.

氧化作用对耐药癌症干细胞中 mTORC 与线粒体蛋白串扰的影响。

Impact of oxytosis on the cross-talk of mTORC with mitochondrial proteins in drug-resistant cancer stem cells.

发表日期:2024 Aug 26
作者: Santhi L Pandrangi, Prasanthi Chittineedi, Ram K Manthari, Balaji Suhruth
来源: JOURNAL OF CELLULAR PHYSIOLOGY

摘要:

通过提供环境输入来运输营养物质和生长因子,雷帕霉素机械靶标 (mTOR) 通过线粒体翻译调节许多基本细胞过程,如自噬、蛋白质合成,在真核细胞的生长和代谢中发挥着重要作用。蛋白质转录因子 A 线粒体、线粒体核糖体蛋白和线粒体呼吸复合物 I
By delivering the environmental inputs to transport nutrients and growth factors, Mechanistic Target of Rapamycin (mTOR) plays a significant role in the growth and metabolism of eukaryotic cells through the regulation of numerous elementary cellular processes such as autophagy, protein synthesis, via translation of mitochondrial protein transcription factor A mitochondrial, mitochondrial ribosomal proteins, and mitochondrial respiratory complexes I &V that are encoded in the nucleus with the help of translation initiation factor 4E-BP. These mitochondrial proteins are involved in cell signaling to regulate proper cell growth, proliferation, and death which are essential for tumor growth and proliferation. This suggests that tumor cells are dependent on mTORC1 for various metabolic pathways. However, this crucial regulator is activated and regulated by calcium homeostasis. Mounting evidence suggests the role of calcium ions in regulating mitochondrial enzymes and proteins. Hence, disrupting calcium homeostasis leads to calcium-dependent cell death called "Oxytosis" through hampering the expression of various mitochondrial proteins. "Oxytosis" is a novel non-apoptotic cell death characterized by glutamate cytotoxicity and ferritin degradation. The present review focuses on the crosstalk between mTORC1 and mitochondrial proteins in the cancer pathophysiology and the impact of calcium ions on disrupting mTORC1 leading to the induction of "Oxytosis."© 2024 The Author(s). Journal of Cellular Physiology published by Wiley Periodicals LLC.