Expression data from U-87 human glioma cells with proficient and deficient NF-B after treatment with temozolomide

The transcription factor, NF-B, plays a central role in the response to DNA damage. This ubiquitous family of proteins is made up of five subunits: p50 (NF-B1, p105), p52 (NF-B2, p100), p65 (relA), relB, and crel that appear in their mature form as dimers. Following stimulation, NF-B dimers translocate to the nucleus where they bind specific consensus elements (B-sites) in the promoter region of genes involved in cell survival, inflammation and the immune system. While there is a general propensity of NF-B to mediate survival, this is not always the case and several reports note the pro-apoptotic nature of the NF-B pathway. In examining the NF-B response to DNA damage, we have found that the p50 subunit plays a central role in modulating cytotoxicity following TMZ treatment in malignant glioma. In the current study, given the importance of p50 to the cytotoxic response to TMZ, we set out to identify NF-B-dependent factors that modulate the response to TMZ.

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