| 中文关键词: 内质网应激 未折叠蛋白反应 癌症进展 |
| 英文关键词:endoplasmic reticulum stress unfolded protein response cancer progression |
| 基金项目:国家自然科学基金（81770169；81670123） |
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| 摘要点击次数: 1922 |
| 全文下载次数: 335 |
| 中文摘要: |
| 摘 要：内质网是真核细胞中控制蛋白质合成、折叠和加工的主要细胞器。在内质网应激条件下，错误折叠的蛋白质在该细胞器中积累，当错误折叠的蛋白质积累超过临界阈值时，启动称为未折叠蛋白反应（the unfolded protein response，UPR）的信号转导途径，以恢复体内平衡。肿瘤细胞经常暴露于改变蛋白质稳态的因素，从而产生内质网应激。大多数现有的证据支持内质网应激条件下启动UPR信号参与肿瘤细胞的生存和适应应激环境，然而最近的研究结果表明，UPR也可能独立于蛋白质错误折叠而参与癌症的进展。全文主要综述UPR在癌症进展中的作用，为癌症治疗潜在靶点提供思路。 |
| 英文摘要: |
| Abstract：The endoplasmic reticulum(ER) is a principal intracellular organelle responsible for protein synthesis，folding and processing in eukaryotic cells. In ER stress conditions，misfolded proteins accumulate in this organelle. When misfolded proteins accumulate above a critical threshold，it activates a signal transduction pathway called the unfolded protein response(UPR) within the cell to restore homeostasis. Tumor cells are often exposed to intrinsic and external factors that alter protein homeostasis，thus producing endoplasmic reticulum(ER) stress. Most of the available evidence supports a concept where ER stress signaling is involved in the survival and adaptation of cancer cells to stress conditions；however，recent findings indicate that the UPR may also contribute to cancer independently of protein misfolding. This review mainly describes the activity of UPR involved in tumorigenesis and provides potential targets to cancer therapy. |
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