The regulation of mTORC2 component Rictor under cell stress

• Main Authors: Deng-Fong Chao, 趙登豐
• Other Authors: Mei-Yu Chen
• Format: Others
• Language: zh-TW
• Published: 2019
• Online Access: http://ndltd.ncl.edu.tw/handle/5w2ern

碩士 === 國立陽明大學 === 生化暨分子生物研究所 === 107 === The mechanistic (or mammalian) target of rapamycin (mTOR) is the target protein of a small molecule drug rapamyin, and has been shown to complex with Raptor and Rictor in forming two unique complexes, mTORC1 and mTORC2, respectively. In human cells, mTOR complexes are activated or inhibited while they receive specific signals, regulating diverse signal transduction pathways and thereby influencing growth, metabolism, survival and migration of cells. Previous studies in the literature have uncovered many mTORC1 upstream and downstream signaling pathways and cellular functions. In contrast, very limited knowledge is available concerning Rictor/mTORC2 signaling, especially its upstream regulatory mechanisms. In this thesis study, we have demonstrated that the expression of the mTORC2 component protein Rictor in cancer cells can be influenced under specific cell stress conditions, and Rictor expression may be regulated through transcriptional but not translational control. We have further investigated that mTORC2 down-stream functions and substrates were influenced under cell stress conditions. Here, we have obtained evidence hinting that cell stress may act as an upstream regulatory signal to control Rictor expression and mTORC2 functions in cancer cells.