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RELT induces cellular death in HEK 293 epithelial cells

John K Cusick1, Andrea Mustian, Kate Goldberg

  • 1University of Colorado Denver School of Dental Medicine, Department of Craniofacial Biology, 12801 East 17th Avenue, Aurora, CO 80045, USA. john.cusick@ucdenver.edu

Cellular Immunology
|December 9, 2009
PubMed

Insights

Tumor Necrosis Factor Receptor RELT and its homologues RELL1/RELL2 induce apoptosis in HEK 293 cells. This cell death pathway, characterized by DNA fragmentation, suggests RELT family members play a role in programmed cell death.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • RElT is a novel Tumor Necrosis Factor Receptor.
  • RELL1 and RELL2 are human homologues of RELT.

Purpose of the Study:

  • To investigate the role of RELT and its homologues in inducing cell death.
  • To determine if RELT family members activate apoptotic pathways.

Main Methods:

  • Transient transfection of RELT family members into HEK 293 and COS-7 cells.
  • Observation of cellular morphology changes.
  • Assessment of DNA fragmentation as an indicator of apoptosis.

Main Results:

  • Transfection of RELT, RELL1, and RELL2 into HEK 293 cells induced cell death with DNA fragmentation, indicative of apoptosis.
  • Overexpression of RELT in COS-7 cells caused cell rounding and lifting but no DNA fragmentation.
  • The cellular response to RELT signaling varied between cell types.

Conclusions:

  • RElT and its homologues can induce apoptosis in HEK 293 epithelial cells.
  • The apoptotic effects of RELT signaling may be cell-type specific.
  • RElT family members are implicated in the regulation of programmed cell death.

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