Cyclin D1 is a key regulator of cell proliferation and its expression is subject to both transcriptional and post-transcriptional regulation. In different cellular contexts, different pathways assume a dominant role in regulating its expression, whereas their disregulation can contribute to overexpression of cyclin D1 in tumorigenesis. Here, we discuss the ability of the NF-kappaB (nuclear factor kappaB)/IKK [IkappaB (inhibitor of NF-kappaB) kinase] pathways to regulate cyclin D1 gene transcription and also consider the newly discovered role of the SNARP (SNIP1/SkIP-associated RNA processing) complex as a co-transcriptional regulator of cyclin D1 RNA stability.

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RelA (p65) phosphorylation at threonine 505 acts as a negative regulator of NF-κB function. In addition to its role in regulation of cell death, a role is demonstrated for T505 phosphorylation in regulating autophagy, proliferation, and migration. NOXA is also identified as a downstream, T505-dependent effector of RelA in cell death.