FIGURE 3 | Roles of galectins in tumorigenesis.

Galectins might have important roles during different steps of tumorigenic processes, including tumour cell transformation, cell-cycle regulation and apoptosis. a | Galectin-1 (Gal-1) and Gal-3 can mediate neoplastic transformation by interacting with oncogenes, such as oncogenic Ras (HRAS and KRAS shown here), and promote Ras-mediated signal transduction (shown here to involve RAF1, extracellular signal-regulated kinase (ERK) 1/2, phosphatidylinositol-3-kinase (PI3K) and the serine/threonine kinase AKT). b | Galectins can also control tumour progression by modulating cell-cycle progression. In particular, Gal-3 regulates the levels of known cell-cycle regulators (including cyclin A, E and D), as well as the cell-cycle inhibitors p21 (WAF 1) and p27 (KIP1), resulting in cell cycle arrest. Gal-1 and Gal-12 induce arrest at various stages of the cell cycle, although the molecular mechanisms of this have not been elucidated. c | Galectins regulate apoptosis. Gal-1 and Gal–9 can induce tumour cell apoptosis when added exogenously to the cell, whereas Gal-7 and Gal-12 promote apoptosis through intracellular mechanisms. Gal-3 has anti-apoptotic functions and it translocates to the perinuclear membrane and to the mitochondria in cells exposed to apoptotic stimuli. The translocation is dependent on synexin, a phospholipid- and Ca²⁺-binding protein, which has been identified as one of the Gal-3-interacting proteins. Gal-3 might also function by interacting with intracellular apoptosis regulators such as B-cell lymphoma 2 (BCL2), or might facilitate the localization of BCL2 to the mitochondria, although definitive evidence for such a function is lacking. The effect of Gal-3 in the regulation of apoptosis depends on its subcellular localization: cytoplasmic Gal-3 is anti-apoptotic, whereas nuclear Gal-3 is pro-apoptotic.

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