Galectin-3 induces cell migration via a calcium-sensitive MAPK/ERK1/2 pathway
PDF | HTML | How to cite
Metrics: PDF 3117 views | HTML 2742 views | ?
Xiaoge Gao1,2,*, Vitaly Balan1,3,*, Guihua Tai2, Avraham Raz1
1 Department of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA
2 School of Life Sciences, Northeast Normal University, Changchun, PR China
3 Present address: Everon Biosciences, Buffalo, NY
* These authors contributed equally to the work
Avraham Raz, email:
Keywords: galectin-3, calcium ions, protein kinase C, extracellular signal regulated protein kinase1/2, cell migration
Received: January 15, 2014 Accepted:February 17, 2014 Published: February 19, 2014
The presence and level of circulating galectin-3 (Gal-3), a member of the galectin family, is associated with diverse diseases ranging from heart failure, immune disorders to cancer metastasis and serves as a biomarker of diagnosis and treatment response. However, the mechanisms by which exogenous Gal-3 affects pathobiology events remain elusive. In the current study, we found that exogenous Gal-3 slightly delays, while prolonging tyrosine phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in HeLa cells through a calcium-sensitive and PKC-dependent signaling pathway. The activation was dependent on the sugar-binding properties of Gal-3, since the antagonist lactose could inhibit it. The sugar-binding motif of Gal-3 was required for the activation of ERK1/2. The activation of ERK1/2 was necessary for the initiation and induction of cell migration associated with the phosphorylation of paxillin. All the results presented in this study suggest a novel calcium-sensitive and PKC-dependent pathway through which circulating Gal-3 promotes cell migration and activating the ERK1/2. Taken together, the data depicted here propose a biological function and a target for the diseases’ associated circulating Gal-3.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.