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In vivo activation of STAT3 in cutaneous T-cell lymphoma. Evidence for an antiapoptotic function of STAT3

V H Sommer1, O J Clemmensen, O Nielsen

  • 1Institutes of Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark.

Leukemia
|May 14, 2004
PubMed

Insights

Signal transducer and activator of transcription 3 (STAT3) is activated in advanced mycosis fungoides (MF) and cutaneous T-cell lymphoma (CTCL) tumors. STAT3 activation protects malignant cells from apoptosis, suggesting it drives MF/CTCL progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Dermatology

Background:

  • Neoplastic transformation involves oncogenic protein activation.
  • Signal transducers and activators of transcription (STAT) proteins play roles in cell signaling and cancer.
  • Mycosis fungoides (MF) and cutaneous T-cell lymphoma (CTCL) are types of T-cell lymphoma affecting the skin.

Purpose of the Study:

  • To investigate the role of STAT3 activation in the pathogenesis of MF/CTCL.
  • To determine if STAT3 activation correlates with disease stage in MF/CTCL.
  • To assess the impact of STAT3 on the survival of CTCL tumor cells.

Main Methods:

  • Immunohistochemical analysis of activated STAT3 (p-STAT3) in MF/CTCL lesions.
  • Transfection of CTCL tumor cells with wild-type STAT3 (STAT3wt) or dominant-negative STAT3 (STAT3D).
  • Assessment of apoptosis in transfected CTCL cells.

Main Results:

  • Constitutive STAT3 activation was frequent in malignant lymphocytes of advanced CTCL tumors.
  • STAT3 activation was minimal in early-stage MF lesions (patch and plaque stages).
  • Inhibition of STAT3 (using STAT3D) significantly increased apoptosis in CTCL tumor cells, while STAT3wt expression had no effect.

Conclusions:

  • STAT3 is significantly activated in advanced MF/CTCL tumors but not in early stages.
  • STAT3 plays a crucial role in protecting CTCL tumor cells from apoptosis.
  • STAT3 is implicated as a key factor in the malignancy and progression of CTCL.

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