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Real Time Detection of In Vitro Tumor Cell Apoptosis Induced by CD8+ T Cells to Study Immune Suppressive Functions of Tumor-infiltrating Myeloid Cells
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LUCA-15 suppresses CD95-mediated apoptosis in Jurkat T cells

L C Sutherland1, M Lerman, G T Williams

  • 1The Henry Hood Research Program, Sigfried and Janet Weis Center for Research, Geisinger Clinic, Danville 17822-2616, USA.

Oncogene
|June 23, 2001
PubMed

Insights

The LUCA-15 gene suppresses programmed cell death (apoptosis) by up-regulating Bcl-2, acting as a selective inhibitor of cell death. This confirms the LUCA-15 locus

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • LUCA-15 is a candidate tumor suppressor gene located at the 3p21.3 lung cancer locus.
  • A splice variant of LUCA-15 was previously shown to promote apoptosis and inhibit T cell proliferation.
  • Antisense cDNA targeting this variant suppressed CD95-mediated apoptosis.

Purpose of the Study:

  • To investigate the role of LUCA-15 itself in regulating apoptosis.
  • To determine the mechanism by which LUCA-15 affects the CD95 signaling pathway.
  • To assess the selectivity of LUCA-15's apoptotic inhibitory function.

Main Methods:

  • Overexpression of LUCA-15 in human Jurkat T cells.
  • Analysis of CD95-mediated apoptosis.
  • Assessment of Bcl-2 protein levels.
  • Induction of apoptosis using staurosporine and etoposide.

Main Results:

  • LUCA-15 overexpression suppressed CD95-mediated apoptosis in Jurkat cells.
  • Apoptosis suppression occurred before the final execution stage of the CD95 pathway.
  • LUCA-15 overexpression led to increased Bcl-2 protein levels.
  • LUCA-15 inhibited staurosporine-induced apoptosis but not etoposide-induced apoptosis.

Conclusions:

  • LUCA-15 acts as a selective inhibitor of programmed cell death.
  • The LUCA-15 gene locus is important for controlling apoptosis.
  • Up-regulation of Bcl-2 is associated with LUCA-15's anti-apoptotic effect.

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