RB and lamins in cell cycle regulation and aging

While speculation has centered on a role for nuclear lamins in tumor progression for many years, most of the diseases that have been linked to lamin mutation are dystrophic in nature, often limiting the proliferation potential of affected cells in vivo and in vitro. Nevertheless, these lamin mutations, particularly in the LMNA gene that encodes A-type lamins, have provided an interesting tool set to understand functions of nuclear intermediate filament proteins in cell cycle progress and various means of exit, including quiescence, senescence, and differentiation down various lineages. The picture that has emerged is complex with lamins controlling the activity of key cell cycle factors such as the retinoblastoma protein (RB) and interacting with several important signal transduction pathways. Here we describe the current state of knowledge and speculate that lamins may be intimately involved in the regulation of cell proliferation, acting at the interface between cancer and aging.