Unraveling galectin-1 as a novel therapeutic target for cancer

Astorgues‐Xerri, Lucile; Riveiro, María E.; Tijeras‐Raballand, Annemilaï; Serova, Maria; Neuzillet, Cindy; Albert, Sébastien; Raymond, Éric; Faivre, Sandrine

doi:10.1016/j.ctrv.2013.07.007

Cited by 182 publications

(194 citation statements)

References 142 publications

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“…It is thus conceivable that Gal‐1‐mediated accumulation of these two potent cyclin‐dependent kinase 2 inhibitors may operate also in reactive glial cells, ultimately arresting them in G1 phase of cell cycle. Besides regulation of cell cycle, exogenously added Gal‐1 also exerts effects through interaction with integrins (Astorgues‐Xerri et al, 2014; Moiseeva et al, 2003), such as activating proapoptotic α5β1‐integrin signaling (Sanchez‐Ruderisch et al, 2011). Gal‐1‐induced apoptosis involves several intracellular mediators including the transcription factor AP1 and the downregulation of Bcl2 protein production (Hahn et al, 2004; Rabinovich et al, 2000; Walzel et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Astrocyte reactivity after brain injury—: The role of galectins 1 and 3

Sirko

Irmler

Gascón

et al. 2015

Glia

107

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Astrocytes react to brain injury in a heterogeneous manner with only a subset resuming proliferation and acquiring stem cell properties in vitro. In order to identify novel regulators of this subset, we performed genomewide expression analysis of reactive astrocytes isolated 5 days after stab wound injury from the gray matter of adult mouse cerebral cortex. The expression pattern was compared with astrocytes from intact cortex and adult neural stem cells (NSCs) isolated from the subependymal zone (SEZ). These comparisons revealed a set of genes expressed at higher levels in both endogenous NSCs and reactive astrocytes, including two lectins—Galectins 1 and 3. These results and the pattern of Galectin expression in the lesioned brain led us to examine the functional significance of these lectins in brains of mice lacking Galectins 1 and 3. Following stab wound injury, astrocyte reactivity including glial fibrillary acidic protein expression, proliferation and neurosphere‐forming capacity were found significantly reduced in mutant animals. This phenotype could be recapitulated in vitro and was fully rescued by addition of Galectin 3, but not of Galectin 1. Thus, Galectins 1 and 3 play key roles in regulating the proliferative and NSC potential of a subset of reactive astrocytes. GLIA 2015;63:2340–2361

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Section: Discussionmentioning

confidence: 99%

Astrocyte reactivity after brain injury—: The role of galectins 1 and 3

Sirko

Irmler

Gascón

et al. 2015

Glia

107

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show abstract

“…GAL1 belongs to a family of carbohydrate-binding proteins, with high affinity for β-galactosides. GAL1 overexpression has been observed in several tumor types, and has been associated with tumor progression (8). GAL1 contains a prenyl-binding pocket, which interacts with the farnesyl group in GTP-HRAS, independently of lectin function.…”

Section: Abstract the Goal Of This Study Was To Develop Combinatoriamentioning

confidence: 99%

Inhibition of Galectin-1 Sensitizes HRAS-driven Tumor Growth to Rapamycin Treatment

Michael

Wurtzel

Goldfinger

2016

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“…However, recent reports indicate that Galectin proteins play a critical role. Galectin over-expression has been observed in several tumor types, and has been associated with tumor progression (46). Galectins are a family of carbohydrate-binding proteins, with high affinity for β-galactosides.…”

Section: Plasma Membrane Targeting Of Rasmentioning

confidence: 99%

“…To investigate a more translational approach taking advantage of Ras plasma membrane microdomain targeting, we considered whether inhibition of Gal-1 would alter HRAS PM membrane microdomain localization, and thereby disrupt CA HRAS in a manner similar to geneticallyenforced HRAS sequestration (i.e., HRAS-tR). We utilized OTX008, a small molecule allosteric inhibitor of Gal-1, which binds on the opposite side from the β-galactoside-binding site, and has been demonstrated as an anticancer agent (46,174,175). We found that OTX008 treatment shifts HRAS to the lipid ordered domain and yields a marked inhibition of tumor growth.…”

Section: Gal-1 and Combinatorial Inhibitionmentioning

confidence: 99%