Re-expression of senescent markers in deinduced reversibly immortalized cells

Exp Gerontol. 1992 Sep-Dec;27(5-6):477-92. doi: 10.1016/0531-5565(92)90003-i.

Abstract

We have developed a simian virus 40 (SV40) T-antigen immortalized human cell line, 1MR90-D305.2H4 (IDH4), in which the expression of T-antigen is controlled by the mouse mammary tumor virus (MMTV) promoter and thus regulated by steroids such as dexamethasone. Studies on the regulation of proliferation by T-antigen led to the formulation of a two-stage model for human cell immortalization, in which a mortality stage 1 mechanism (M1) was the target of T-antigen action, and an independent mortality stage 2 mechanism (M2) produced crisis and prevented T-antigen from directly immortalizing cells. Rarely, a cell expressing T-antigen escaped crisis (e.g., M2) and was capable of indefinite proliferation. This model predicted that the deinduction of T-antigen in IDH4 cells would lead to the reexpression of the M1 mechanism, and thus a reexpression of the senescent phenotype. Our study confirms the prediction that, in the absence of steroids, IDH4 cells express a variety of morphological and biochemical markers characteristic of normal senescent human fibroblasts.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antigens, Viral, Tumor / genetics
  • Antigens, Viral, Tumor / metabolism
  • Base Sequence
  • Cell Division
  • Cell Line, Transformed
  • Cellular Senescence / physiology*
  • DNA / biosynthesis
  • Dexamethasone / pharmacology
  • Fibroblasts / cytology*
  • Fibroblasts / drug effects
  • Fibroblasts / immunology
  • Gene Expression
  • Humans
  • Mammary Tumor Virus, Mouse / genetics
  • Molecular Sequence Data
  • Plasminogen Activator Inhibitor 1 / biosynthesis
  • Plasminogen Activator Inhibitor 1 / genetics
  • Promoter Regions, Genetic
  • Simian virus 40

Substances

  • Antigens, Viral, Tumor
  • Plasminogen Activator Inhibitor 1
  • Dexamethasone
  • DNA