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Galectin-3 induces cell migration via a calcium-sensitive MAPK/ERK1/2 pathway.

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Circulating galectin-3 (Gal-3) activates extracellular signal-regulated kinase 1/2 (ERK1/2) via a calcium-sensitive pathway, promoting cell migration. This finding reveals a novel mechanism for Gal-3

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Circulating galectin-3 (Gal-3) is a biomarker for various diseases, including cancer metastasis.
  • The precise mechanisms by which exogenous Gal-3 influences disease pathobiology are not fully understood.

Purpose of the Study:

  • To elucidate the signaling pathways by which exogenous Gal-3 affects cellular events.
  • To investigate the role of Gal-3 in regulating extracellular signal-regulated kinase 1/2 (ERK1/2) activation and cell migration.

Main Methods:

  • HeLa cells were treated with exogenous Gal-3.
  • Tyrosine phosphorylation of ERK1/2 and paxillin was assessed.
  • Calcium sensitivity and protein kinase C (PKC) dependence were evaluated.
  • The role of Gal-3's sugar-binding motif was tested using lactose.

Main Results:

  • Exogenous Gal-3 induced a calcium-sensitive and PKC-dependent tyrosine phosphorylation of ERK1/2.
  • Gal-3's sugar-binding properties, specifically its sugar-binding motif, were essential for ERK1/2 activation.
  • ERK1/2 activation was necessary for Gal-3-induced cell migration, evidenced by paxillin phosphorylation.

Conclusions:

  • Circulating Gal-3 activates a novel calcium-sensitive and PKC-dependent pathway.
  • This pathway involves ERK1/2 activation and promotes cell migration.
  • These findings suggest a potential therapeutic target for diseases associated with circulating Gal-3.