Down-regulation of statin, a nonproliferation-specific nuclear protein, and up-regulation of c-myc after initiation of programmed cell death in mouse fibroblasts.

Published

Journal Article

Deprivation of growth factors has been shown to induce programmed cell death in many cell types, including mouse 3T3 fibroblasts. Programmed cell death (apoptosis) is an active process of self-destruction which is thought to require the expression of unique genes. Recently, the expression of cell cycle genes such as c-fos and c-myc, and re-entrance to cell cycle traverse, are thought to be necessary to induce programmed cell death. Previous work in this laboratory has shown that statin is a nonproliferation-specific nuclear protein present in the nuclei of young quiescent or senescent human fibroblasts, as well as in growth-arrested mouse 3T3 fibroblasts; we have reported that statin disappears rapidly after the blockage of growth arrest is removed and cells are allowed to resume cell cycle traverse. In this report we address the question of whether cells induced to enter the programmed cell death process also lose the expression of statin. We studied density-arrested quiescent mouse 3T3 cells, which undergo rapid cell death by apoptosis upon serum deprivation. Our results suggest that c-myc expression is induced, as previously reported in other systems of apoptotic death. Interestingly, we also find that statin indeed disappears after the induction of programmed cell death is initiated. These results further support the notion that when apoptosis is induced, cells behave as though released from replication arrest, and experience some part of the G1 phase of the cell cycle. The difference between this event and normal cell cycle traverse is that this experience of the G1 phase in the apoptotic process is an abortive one, with the end result of cell demise.

Full Text

Duke Authors

Cited Authors

  • Wang, E; Pandey, S

Published Date

  • April 1995

Published In

Volume / Issue

  • 163 / 1

Start / End Page

  • 155 - 163

PubMed ID

  • 7896892

Pubmed Central ID

  • 7896892

International Standard Serial Number (ISSN)

  • 0021-9541

Digital Object Identifier (DOI)

  • 10.1002/jcp.1041630118

Language

  • eng

Conference Location

  • United States