Interdisciplinary Cluster for Applied Genoproteomics (GIGA), Centre Hospitalier Universitaire (CHU), Sart-Tilman, Liege, Belgium; Laboratory of Medical Chemistry, University of Liege, CHU, Sart-Tilman, Liege, Belgium; GIGA-Signal Transduction, University of Liege, CHU, Sart-Tilman, Liege, Belgium.
Interdisciplinary Cluster for Applied Genoproteomics (GIGA), Centre Hospitalier Universitaire (CHU), Sart-Tilman, Liege, Belgium; Laboratory of Medical Chemistry, University of Liege, CHU, Sart-Tilman, Liege, Belgium; GIGA-Signal Transduction, University of Liege, CHU, Sart-Tilman, Liege, Belgium; Walloon Excellence in Life Sciences and Biotechnology (WELBIO), Wavre, Belgium.
Trends Mol Med. 2015 Jun;21(6):385-93. doi: 10.1016/j.molmed.2015.04.001. Epub 2015 May 13.
Oncogenic proteins cooperate to promote tumor development and progression by sustaining cell proliferation, survival and invasiveness. Constitutive epidermal growth factor receptor (EGFR) and nuclear factor κb (NF-κB) activities are seen in multiple solid tumors and combine to provide oncogenic signals to cancer cells. Understanding how these oncogenic pathways are connected is crucial, given their role in intrinsic or acquired resistance to targeted anticancer therapies. We review molecular mechanisms by which both EGFR- and NF-κB-dependent pathways establish positive loops to increase their oncogenic potential. We also describe how NF-κB promotes resistance to EGFR inhibitors.
致癌蛋白通过维持细胞增殖、存活和侵袭来促进肿瘤的发生和发展。在多种实体肿瘤中均可观察到组成性表皮生长因子受体（EGFR）和核因子κB（NF-κB）的活性，并共同向癌细胞提供致癌信号。鉴于它们在内在或获得性对抗癌靶向治疗的耐药性中的作用，了解这些致癌途径是如何连接的至关重要。我们综述了 EGFR 和 NF-κB 依赖性途径建立正反馈以增加其致癌潜力的分子机制。我们还描述了 NF-κB 如何促进对 EGFR 抑制剂的耐药性。
