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Updated: Jan 31, 2026

Measurement of Natural Killer Cell-Mediated Cytotoxicity and Migration in the Context of Hepatic Tumor Cells
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SAK-HV Promotes RAW264.7 cells Migration Mediated by MCP-1 via JNK and NF-κB Pathways

Yao Chen1, Wen-Liang Fu1, Xiang-Dong Gan1

  • 1Institute of Military Cognitive and Brain Sciences, Beijing, 100850, China.

International Journal of Biological Sciences
|December 27, 2018
PubMed

Insights

SAK-HV protein triggers macrophage migration by activating JNK and NF-κB pathways. This process involves Monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2, revealing new insights into SAK-HV

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Macrophage migration is crucial for immunity and disease.
  • Its regulatory mechanisms are complex and not fully understood.
  • SAK-HV protein has known thrombolytic and lipid-lowering effects.

Purpose of the Study:

  • To investigate the effect of SAK-HV on macrophage migration.
  • To elucidate the molecular pathways involved in SAK-HV-induced macrophage migration.

Main Methods:

  • Utilized RAW264.7 macrophage cell line.
  • Investigated the role of SAK-HV and its SAK-mutant domain.
  • Analyzed the activation of c-jun N-terminal kinases (JNK) and nuclear factor-κB (NF-κB) pathways.
  • Examined the expression of Monocyte chemoattractant protein-1 (MCP-1) and its interaction with Chemokine (C-C motif) Receptor 2 (CCR2).

Main Results:

  • SAK-HV significantly induced RAW264.7 cell migration.
  • SAK-HV activated both JNK and NF-κB pathways.
  • MCP-1 expression was upregulated by SAK-HV and mediated by JNK/NF-κB.
  • MCP-1 promoted migration via autocrine interaction with CCR2.

Conclusions:

  • SAK-HV induces macrophage migration through its SAK-mutant domain.
  • The JNK and NF-κB pathways are key mediators of this effect.
  • MCP-1 plays a critical role in SAK-HV-driven macrophage migration via CCR2, offering novel pharmacodynamic insights.
Keywords:
JNKMCP-1NF-κBSAK-HVmacrophage migration

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