Nogueira Lorena, Ruiz-Ontañon Patricia, Vazquez-Barquero Alfonso, Moris Francisco, Fernandez-Luna Jose L
Molecular Genetics Unit, Hospital Valdecilla-IFIMAV, Santander, Spain.
Oncotarget. 2011 Aug;2(8):646-53. doi: 10.18632/oncotarget.322.
Cancer initiating cells have been described to be the only cell population with tumorigenic capacity in glioblastoma multiforme, one of the most aggressive and untreatable cancers. Recent work from our group described that NFκB pathway was activated in glioblastoma initiating cells undergoing differentiation, and that blockade of this activation promoted senescence of differentiating cells. NFκB activation in cancer may be the result of either exposure to proinflammatory stimuli in the tumor microenvironment or upregulation of the signaling pathway by upstream regulators. Appropriate control of NFκB activity, which can be achieved by gene modification or pharmacological strategies, would provide a potential approach for the management of NFκB related tumors, including glioblastoma. Here, we summarize the current knowledge of the relevance of NFκB in cancer and its possible role as a target of therapeutic intervention..
癌症起始细胞被认为是多形性胶质母细胞瘤中唯一具有致瘤能力的细胞群体，多形性胶质母细胞瘤是最具侵袭性且难以治疗的癌症之一。我们团队最近的研究表明，在经历分化的胶质母细胞瘤起始细胞中，NFκB通路被激活，并且阻断这种激活会促进分化细胞的衰老。癌症中NFκB的激活可能是肿瘤微环境中促炎刺激暴露的结果，或者是上游调节因子对信号通路的上调所致。通过基因修饰或药理学策略实现对NFκB活性的适当控制，将为包括胶质母细胞瘤在内的NFκB相关肿瘤的治疗提供一种潜在方法。在此，我们总结了目前关于NFκB在癌症中的相关性及其作为治疗干预靶点的可能作用的知识。
