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Expression of galectin‐3 in neuronally differentiating PC12 cells is regulated both via Ras/MAPK‐dependent and –independent signalling pathways

Galectin‐3 (gal‐3) is a member of the galectin family of lectins whose expression strongly depends on the cellular state. Here we show that in PC12 cells the expression of gal‐3 protein is regulated via Ras‐ and mitogen‐activated protein kinase (MAPK)‐dependent and independent signalling pathways and correlates with nerve growth factor (NGF)‐mediated neuronal differentiation. Gal‐3 expression, activation of the MAPK ERK1/2 and neurite outgrowth are induced by NGF and basic fibroblast growth factor (bFGF), but not by ciliary neurotrophic factor (CNTF), epidermal growth factor, insulin or interleukin‐6 (IL‐6). In addition, in NGF‐treated PC12 cells, gal‐3 expression, ERK1/2 activation and neurite outgrowth could be specifically inhibited at the level of TrkA, Ras and MAPK‐kinase, whereas expression of an oncogenic form of Ras leads to gal‐3 expression and neurite outgrowth in the absence of growth factors. In NGF‐primed PC12 cells, subsequent treatment with CNTF or IL‐6 induces ERK1/2 activation and neurite outgrowth, but not gal‐3 expression. Treatment of PC12 cells with staurosporine induces gal‐3 expression and neurite outgrowth without ERK1/2 activation. NGF‐ and staurosporine‐induced gal‐3‐expression is also regulated at the transcriptional level. Our data suggest the presence of complex induction mechanisms of gal‐3 expression in neuronally differentiating PC12 cells involving NGF‐, but not CNTF‐ and IL‐6‐driven (in NGF‐primed cells) Ras/MAPK‐related signalling pathways. Staurosporine, in contrast, induces gal‐3 expression by a Ras/MAPK‐independent mechanism.