White Danielle E, Burchill Susan A
Candlelighter's Children's Cancer Research Group, Leeds Institute of Molecular Medicine, Cancer Research UK Clinical Centre, St James's University Hospital, Leeds, UK.
Cancer Lett. 2008 Sep 18;268(2):212-24. doi: 10.1016/j.canlet.2008.03.045. Epub 2008 May 8.
The role of NF-kappaB in the Ewing's sarcoma family of tumours (ESFT) and their response to fenretinide has been investigated. Basal levels of phosphorylated NF-kappaB were low in all ESFT cells. BAY 11-7082 decreased cell viability, which was accompanied by caspase-3 cleavage. This was independent of the increase in reactive oxygen species, p38(MAPK) phosphorylation and expression of NF-kappaB target proteins. NF-kappaB knockdown did not induce death under normal growth conditions, but did reduce TNFalpha-dependent cell survival. Fenretinide-induced apoptosis was independent of NF-kappaB. BAY 11-7082-induced cell death through an NF-kappaB-independent mechanism and enhanced cell death when combined with fenretinide.
已对核因子-κB（NF-κB）在尤因肉瘤家族性肿瘤（ESFT）中的作用及其对芬维A胺的反应进行了研究。在所有ESFT细胞中，磷酸化NF-κB的基础水平较低。BAY 11-7082降低细胞活力，并伴有半胱天冬酶-3的裂解。这与活性氧增加、p38（丝裂原活化蛋白激酶）磷酸化及NF-κB靶蛋白的表达无关。在正常生长条件下，NF-κB敲低不会诱导细胞死亡，但会降低肿瘤坏死因子α（TNFα）依赖性细胞存活。芬维A胺诱导的细胞凋亡与NF-κB无关。BAY 11-7082通过一种不依赖NF-κB的机制诱导细胞死亡，并且与芬维A胺联合使用时可增强细胞死亡。
