Department of Biological, Chemical and Pharmaceutical Science and Technology (STEBICEF), University of Palermo, 90128 Palermo, Italy.
Int J Mol Sci. 2020 Apr 27;21(9):3070. doi: 10.3390/ijms21093070.
Multidrug resistance (MDR), of the innate and acquired types, is one of major problems in treating tumor diseases with a good chance of success. In this review, we examine the key role of nuclear factor-kappa B (NF-κB) to induce MDR in three tumor models characterized precisely by innate or acquired MDR, in particular triple negative breast cancer (TNBC), hepatocellular carcinoma (HCC), and acute myeloid leukemia (AML). We also present different pharmacological approaches that our group have employed to reduce the expression/activation of this transcriptional factor and thus to restore chemo-sensitivity. Finally, we examine the latest scientific evidence found by other groups, the most significant clinical trials regarding NF-κB, and new perspectives on the possibility to consider this transcriptional factor a valid drug target in neoplastic diseases.
多药耐药(MDR),包括先天和获得性耐药,是成功治疗肿瘤疾病的主要问题之一。在这篇综述中,我们研究了核因子-κB(NF-κB)在三种肿瘤模型中诱导 MDR 的关键作用,这些模型分别具有先天或获得性 MDR 的特征,特别是三阴性乳腺癌(TNBC)、肝细胞癌(HCC)和急性髓细胞白血病(AML)。我们还介绍了我们小组采用的不同药理学方法来降低这种转录因子的表达/激活,从而恢复化疗敏感性。最后,我们研究了其他小组发现的最新科学证据、关于 NF-κB 的最重要的临床试验,以及将这种转录因子视为肿瘤疾病有效药物靶点的新观点。