Research Papers:

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

Xiaoge Gao, Vitaly Balan, Guihua Tai and Avraham Raz _

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Oncotarget. 2014; 5:2077-2084. https://doi.org/10.18632/oncotarget.1786

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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.

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PII: 1786