Aspirin Prevention of Colorectal Cancer: Focus on NF-κB Signalling and the Nucleolus
AbstractOverwhelming evidence indicates that aspirin and related non-steroidal anti-inflammatory drugs (NSAIDs) have anti-tumour activity and the potential to prevent cancer, particularly colorectal cancer. However, the mechanisms underlying this effect remain hypothetical. Dysregulation of the nuclear factor-kappaB (NF-κB) transcription factor is a common event in many cancer types which contributes to tumour initiation and progression by driving expression of pro-proliferative/anti-apoptotic genes. In this review, we will focus on the current knowledge regarding NSAID effects on the NF-κB signalling pathway in pre-cancerous and cancerous lesions, and the evidence that these effects contribute to the anti-tumour activity of the agents. The nuclear organelle, the nucleolus, is emerging as a central regulator of transcription factor activity and cell growth and death. Nucleolar function is dysregulated in the majority of cancers which promotes cancer growth through direct and indirect mechanisms. Hence, this organelle is emerging as a promising target for novel therapeutic agents. Here, we will also discuss evidence for crosstalk between the NF-κB pathway and nucleoli, the role that this cross-talk has in the anti-tumour effects of NSAIDs and ways forward to exploit this crosstalk for therapeutic purpose. View Full-Text
A printed edition of this Special Issue is available here.
Share & Cite This Article
Chen, J.; Stark, L.A. Aspirin Prevention of Colorectal Cancer: Focus on NF-κB Signalling and the Nucleolus. Biomedicines 2017, 5, 43.
Chen J, Stark LA. Aspirin Prevention of Colorectal Cancer: Focus on NF-κB Signalling and the Nucleolus. Biomedicines. 2017; 5(3):43.Chicago/Turabian Style
Chen, Jingyu; Stark, Lesley A. 2017. "Aspirin Prevention of Colorectal Cancer: Focus on NF-κB Signalling and the Nucleolus." Biomedicines 5, no. 3: 43.
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.