Therapeutic targeting of cellular stress responses in cancer.
Therapeutic targeting of cellular stress responses in cancer.
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DOI：
10.1111/1759-7714.12890
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发表时间：
2018-12
期刊：
影响因子：
2.9
通讯作者：
Xie S
中科院分区：
文献类型：
--
作者：
Chen M;Xie S
与细菌、酵母和其他已经进化出应对环境压力的途径的生物体类似，癌细胞也发展出增加遗传多样性的机制，以促进适应各种压力条件，包括缺氧、营养匮乏、暴露于DNA损伤剂和免疫反应。为了生存，癌细胞触发驱动基因组不稳定性和突变的机制，改变基因表达程序，并重新编程代谢途径以逃避生长抑制信号和免疫监视。更深入地了解癌细胞克服压力的分子机制将使我们能够开发更有效的癌症治疗策略。在此，我们概述了几个关键的压力施加在癌细胞上，包括氧化，代谢，机械和遗传毒性，并讨论了驱动癌细胞反应的机制。还考虑了这些反应的治疗意义，因为这些因素为靶向压力适应途径铺平了道路，以减缓癌症进展并阻止对治疗的抵抗。
Similar to bacteria, yeast, and other organisms that have evolved pathways to respond to environmental stresses, cancer cells develop mechanisms that increase genetic diversity to facilitate adaptation to a variety of stressful conditions, including hypoxia, nutrient deprivation, exposure to DNA‐damaging agents, and immune responses. To survive, cancer cells trigger mechanisms that drive genomic instability and mutation, alter gene expression programs, and reprogram the metabolic pathways to evade growth inhibition signaling and immune surveillance. A deeper understanding of the molecular mechanisms that underlie the pathways used by cancer cells to overcome stresses will allow us to develop more efficacious strategies for cancer therapy. Herein, we overview several key stresses imposed on cancer cells, including oxidative, metabolic, mechanical, and genotoxic, and discuss the mechanisms that drive cancer cell responses. The therapeutic implications of these responses are also considered, as these factors pave the way for the targeting of stress adaption pathways in order to slow cancer progression and block resistance to therapy.
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