Immortalized mouse embryo fibroblasts are resistant to miR-290-induced senescence regardless of p53 status

Physiol Genomics. 2011 Oct 20;43(20):1153-9. doi: 10.1152/physiolgenomics.00064.2011. Epub 2011 Aug 16.


The prosenescence role of miR-290 and nocodazole has been documented in primary mouse embryo fibroblasts (MEF), while it is not clear whether immortal murine fibroblasts are still responsive to these senescence inducing stimuli. To establish this point, immortal murine fibroblasts with functional (NIH3T3) or nonfunctional p53 (I-MEF) and low levels of miR-290 were tested for their capability to undergo senescence after exposure to either nocodazole or miR-290. Our results clearly indicate that nocodazole induces senescence only in NIH3T3 cells with a functional p53 but not in I-MEF lacking a functional p53. miR-290 overexpression is unable to address any of the tested immortalized clones toward senescence, regardless of the p53 status, suggesting that the prosenescence role of miR-290 is specific for primary but not for immortal murine fibroblasts. Moreover our findings suggest that the mere downregulation of a potential tumor suppressor miRNA in a given cell type does not necessarily imply that it behaves as a tumor suppressor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Transformed
  • Cellular Senescence / drug effects
  • Cellular Senescence / genetics*
  • Clone Cells
  • Embryo, Mammalian / cytology*
  • Fibroblasts / cytology*
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism*
  • Mice
  • MicroRNAs / metabolism*
  • NIH 3T3 Cells
  • Nocodazole / pharmacology
  • Transfection
  • Tumor Suppressor Protein p53 / metabolism*


  • MIRN290 microRNA, mouse
  • MicroRNAs
  • Tumor Suppressor Protein p53
  • Nocodazole