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Updated: Aug 19, 2025

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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Interleukin-1β triggers matrix metalloprotease-3 expression through p65/RelA activation in melanoma cells

Junichi Nunomura1, Rei Nakano1,2,3, Atsuto Naruke1

  • 1Laboratories of Veterinary Radiotherapy, Nihon University College of Bioresource Sciences, Fujisawa, Kanagawa, Japan.

Plos One
|November 29, 2022
PubMed

Insights

Interleukin-1β (IL-1β) increases matrix metalloprotease-3 (MMP-3) in canine melanoma cells, promoting tumor cell migration. This process involves the nuclear factor-kappa B (NF-κB) pathway, specifically p65/RelA activation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Veterinary Medicine

Background:

  • Melanoma is an aggressive skin cancer characterized by local invasion and metastasis.
  • Matrix metalloprotease-3 (MMP-3) degrades extracellular matrix components, facilitating tumor invasion and development.
  • Interleukin-1β (IL-1β) is a pro-inflammatory cytokine implicated in various cancers.

Purpose of the Study:

  • To investigate the role of IL-1β in regulating MMP-3 expression and canine melanoma cell migration.
  • To elucidate the signaling pathway involved in IL-1β-induced MMP-3 expression.

Main Methods:

  • Canine melanoma cells were treated with IL-1β.
  • MMP-3 expression and activity were measured using quantitative real-time PCR and enzyme activity assays.
  • Cell migration was assessed using a wound healing assay.
  • Inhibitors of MMP-3 (UK356618) and NF-κB (TPCA-1) were used.
  • Western blotting was performed to detect protein phosphorylation.
  • Gene silencing of NF-κB subunits (p65/RelA and p105) was conducted.

Main Results:

  • IL-1β treatment significantly increased MMP-3 mRNA expression and enzyme activity in canine melanoma cells.
  • IL-1β induced melanoma cell migration, which was reduced by MMP-3 inhibition.
  • NF-κB pathway activation, indicated by p65/RelA and p105 phosphorylation, was observed upon IL-1β treatment.
  • Inhibition of NF-κB signaling by TPCA-1 suppressed IL-1β-induced MMP-3 expression.
  • Depletion of p65/RelA, but not p105, abolished IL-1β-mediated MMP-3 mRNA upregulation.

Conclusions:

  • IL-1β stimulates MMP-3 expression and promotes migration in canine melanoma cells.
  • The IL-1β-induced MMP-3 expression is mediated through the activation of the NF-κB pathway, specifically involving the p65/RelA subunit.
  • Targeting the IL-1β/NF-κB/MMP-3 axis may represent a therapeutic strategy for canine melanoma.

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