Protocol

Inflammation and Cancer

Volume 512 of the series Methods in Molecular Biology™ pp 99-117

Analysis of the TLR/NF-κB Pathway in Antigen-Presenting Cells in Malignancies Promoted by Inflammation

  • J. Magarian BlanderAffiliated withDepartment of Medicine, Immunology Institute, Mount Sinai School of Medicine

* Final gross prices may vary according to local VAT.

Get Access

Summary

Activation of the transcription factor, nuclear factor of κB (NF-κB), has recently emerged as the critical link between inflammation and cancer. NF-κB is activated by many signals including DNA damage and microbial pathogen recognition. Although microbial infections account for an estimated 15% of all cancer related deaths, NF-κB is constitutively activated in various types of cancer as a direct result of chromosomal translocations, deletions and mutations affecting both NF-κB and its regulators. NF-κB exerts the transcriptional activation and repression of inflammatory and immune response genes as well as genes mediating cell survival and proliferation, and thus stands to impact various cellular processes. The decision is made through the integration of the pathway of NF-κB activation with a complex array of cell signaling networks that are at present poorly understood. Here, two methods are presented, protein co-immunoprecipitation and subcellular co-localization by immunofluorescence microscopy, to help investigations into the links between NF-κB-induced inflammation and cancer. Understanding the details of these pathways will aid in the development of new diagnostic and therapeutic applications.

Key words

Toll-like receptors Pattern recognition receptors Nuclear factor of κB Signal transduction Inflammation Cancer Co-immunoprecipitation; Immunofluoresence microscopy Sub-cellular co-localization Organelle markers