TRIM11 cooperates with HSF1 to suppress the anti-tumor effect of proteotoxic stress drugs |
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| Authors: | Liang Chen |
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| Institution: | 1. Shenzhen Laboratory of Tumor Cell Biology, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, University City of Shenzhen, Shenzhen, P. R. China;2. Department of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA |
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| Abstract: | Cells mainly rely on stress proteins, such as heat-shock proteins (HSPs), to respond to various proteotoxic conditions. These proteins protect tumor cells and enhance their survive. However, the regulation of stress proteins involved in protein quality control (PQC) is still poorly understood. Here, we report that the expression of TRIM11, an important regulator of PQC, is positively correlated with tumor cell surviaval during the proteotoxic conditions induced by anti-tumor drugs. In addition, HSF1 is required for TRIM11-mediated removal of protein aggregates and resistance of proteotoxic stress. During these processes, TRIM11 interacts with and stabilizes HSF1, increaseing HSF1 levels in the nucleus. These findings identify that TRIM11, through cooperation with HSF1, protects cells against the proteotoxic stress and promotes tumor cell survival. |
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| Keywords: | Proteotoxic stress TRIM11 cell viability anti-tumor HSF1 |
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