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Membrane Type-1 Matrix Metalloproteinase Expression in Acute Myeloid Leukemia and Its Upregulation by Tumor Necrosis

Leah A Marquez-Curtis1, Neeta Shirvaikar, A Robert Turner

  • 1Canadian Blood Services R&D, Edmonton, Alberta T6G 2R8, Canada. anna.janowska@blood.ca.

Cancers
|November 12, 2013
PubMed

Insights

Acute myeloid leukemia (AML) cells express membrane type-1 matrix metalloproteinase (MT1-MMP), which enhances tumor invasion. Tumor necrosis factor-alpha (TNF-α) upregulates MT1-MMP, increasing proMMP-2 activation and AML cell migration.

Area of Science:

  • Biochemistry
  • Oncology
  • Cell Biology

Background:

  • Membrane type-1 matrix metalloproteinase (MT1-MMP) is involved in tumor invasion and hematopoietic cell trafficking.
  • MT1-MMP physiologically activates proMMP-2.
  • Tumor necrosis factor-alpha (TNF-α) is elevated in acute myeloid leukemia (AML).

Purpose of the Study:

  • To investigate MT1-MMP expression in primary AML cells.
  • To determine the effect of TNF-α on MT1-MMP expression in AML.
  • To assess the role of MT1-MMP in AML cell invasion and proMMP-2 activation.

Main Methods:

  • Analysis of MT1-MMP mRNA expression in primary AML samples.
  • Co-culture experiments with AML cells and bone marrow stromal cells.
  • Gene silencing of MT1-MMP using siRNA.
  • Treatment with recombinant human TNF-α.
  • Assay of proMMP-2 activation and trans-Matrigel migration.

Main Results:

  • MT1-MMP mRNA was detected in 41 out of 43 primary AML samples.
  • AML cells activated proMMP-2 when co-cultured with stromal cells.
  • MT1-MMP gene silencing inhibited proMMP-2 activation and AML cell migration.
  • Recombinant TNF-α upregulated MT1-MMP expression, enhancing proMMP-2 activation and migration.

Conclusions:

  • AML cells express MT1-MMP, contributing to their invasive potential.
  • TNF-α enhances MT1-MMP expression in AML, leading to increased MMP-2 activation.
  • MT1-MMP and TNF-α are potential therapeutic targets for AML.

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