Vitamin Research Institute, Moscow, Russia, Porto, Portugal.
Aging Dis. 2011 Jun;2(3):219-30. Epub 2010 Feb 20.
This work considers reactive oxygen species (ROS) signaling in solid tumors. Most (probably all) cancer cells are characterized by ROS overproduction that is they exist under conditions of incessant oxidative stress. For example ROS overproduction has been shown in prostate, pancreatic, melanoma, and glioma cells. ROS overproduction has been also demonstrated in breast, liver, bladder, colon, and ovarian cancers. Although these examples probably do not incorporate all the described data concerning ROS overproduction in cancer cells, they clearly support a proposal about enhanced oxidative stress in these cells. Therefore the mechanisms of ROS signaling in the survival and death of cancer cells and comparison with ROS signaling in senescent cells ought to be considered. It might be suggested that ROS overproduction in cancer cells is a major origin of their survival and resistance to anticancer treatment while the enhanced oxidative stress responsible for aging development. However it is of particular interest that additional ROS production by prooxidants can induce apoptosis in cancer cells. We suggest that moderate oxidative stress can stimulate proliferation and survival of cancer sells by conditioning mechanism while the enhancement of ROS overproduction by prooxidants under severe oxidative stress results in apoptosis and cell death. Aging development is always characterized by harmful ROS overproduction although the moderate increase in ROS formation in senescent cells might be not dangerous. Similar double-edged sword effects of ROS might be observed during the development of other pathologies for example diabetes mellitus.
这项工作考虑了活性氧（ROS）在实体瘤中的信号转导。大多数（可能是所有）癌细胞的特点是 ROS 过度产生，也就是说它们存在于持续氧化应激的条件下。例如，已经在前列腺癌、胰腺癌、黑色素瘤和神经胶质瘤细胞中显示出 ROS 过度产生。在乳腺癌、肝癌、膀胱癌、结肠癌和卵巢癌中也已经证明了 ROS 过度产生。尽管这些例子可能没有包含关于癌细胞中 ROS 过度产生的所有描述性数据，但它们清楚地支持了这些细胞中氧化应激增强的观点。因此，应该考虑 ROS 信号转导在癌细胞的存活和死亡中的机制，并将其与衰老细胞中的 ROS 信号转导进行比较。可以认为，癌细胞中 ROS 的过度产生是它们存活和抵抗抗癌治疗的主要来源，而增强的氧化应激则是衰老发展的原因。然而，特别有趣的是，促氧化剂额外产生的 ROS 可以诱导癌细胞凋亡。我们认为，适度的氧化应激可以通过调节机制刺激癌细胞的增殖和存活，而在严重氧化应激下促氧化剂增强 ROS 过度产生会导致细胞凋亡和死亡。衰老的发展总是伴随着有害的 ROS 过度产生，尽管衰老细胞中 ROS 形成的适度增加可能并不危险。在其他病理学的发展过程中，例如糖尿病，可能会观察到类似的双刃剑效应的 ROS。
