Overexpression of MnSOD protects murine fibrosarcoma cells (FSa-II) from apoptosis and promotes a differentiation program upon treatment with 5-azacytidine: Involvement of MAPK and NFκB pathways

Y. Zhao, K. K. Kiningham, S. M. Lin, D. K. St. Clair

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

Stable transfection of neomycin and human manganese superoxide dismutase (MnSOD2) expression plasmids into a murine fibrosarcoma cell line (FSa-II) was previously done in our laboratory. Treatment with 10 μM 5-azacytidine induced apoptosis in the control cell line (NEO), whereas the MnSOD-overexpressing cell line (SOD-H) demonstrated differentiated-appearing morphology. The levels of the myogenic transcription factor, MyoD, and the muscle-specific marker, α-actin, were increased over time with 5-azacytidine treatment in the SOD-H cell line. Nuclear transcription factor NFκB was activated in the SOD-H cell line, whereas inhibition of NFκB activation reduced the levels of MyoD and α-actin. Members of mitogen-activated protein kinase pathway and the Raf1/MEK/ERK cascade were shown to play a positive role in this event. Overexpression of MnSOD not only can protect cells from the toxic effects of 5-azacytidine, but can also promote the fibrosarcoma cells to enter a differentiation program.

Original languageEnglish
Pages (from-to)375-386
Number of pages12
JournalAntioxidants and Redox Signaling
Volume3
Issue number3
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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