Abstract
Accumulating evidence suggests that galectin-3 is a histologic marker of thyroid cancer. However, the pharmacological lectin-based approach has not been well studied. In the present study, we aimed to investigate the therapeutic potential of novel galectin-3 inhibitors by treating thyroid cancer cells with different concentrations of GB1107 or TD139. At high doses, TD139, but not GB1107, reduced cell viability and clonogenicity of thyroid cancer cells. TD139 induced apoptosis of thyroid cancer cells, as evident by an increase in the percentage of sub-G1 cells on cell cycle analysis, caspase-3 activation, and PARP1 cleavage. Either GB1107 or TD139 significantly inhibited cell coherence and counteracted anoikis resistance. Both inhibitors decreased migratory and invasive abilities in a dose-dependent manner. Furthermore, GB1107 and TD139 treatment attenuated AKT phosphorylation and decreased the expression of β-catenin and MMP2. In conclusion, these novel galectin-3 inhibitors suppressed the anoikis resistance, motility, and invasive capacity of thyroid cancer cells at least partly through the AKT/β-catenin pathway. Galectin-3 inhibitors are potentially suitable for preclinical evaluation of treatment and/or prevention of metastatic spread in thyroid cancer.
Highlights
Accumulating evidence suggests that galectin-3 is a histologic marker of thyroid cancer
We aimed to investigate the therapeutic potential of novel galectin3 inhibitors by treating thyroid cancer cells with different concentrations of GB1107 or TD139
FTC-133 and 8505C cells were treated with increasing concentrations of two different galectin-3 inhibitors, GB1107 and TD139, and cell viability was assessed using Cell Counting Kit-8 (CCK-8) assay
Summary
Accumulating evidence suggests that galectin-3 is a histologic marker of thyroid cancer. We aimed to investigate the therapeutic potential of novel galectin inhibitors by treating thyroid cancer cells with different concentrations of GB1107 or TD139. GB1107 and TD139 treatment attenuated AKT phosphorylation and decreased the expression of β-catenin and MMP2 These novel galectin-3 inhibitors suppressed the anoikis resistance, motility, and invasive capacity of thyroid cancer cells at least partly through the AKT/β-catenin pathway. Menachem et al reported that combined treatment with a Ras inhibitor and modified citrus pectin, a water-soluble polysaccharide derived from a citrus fruit that inhibits galectin-3, induced cell cycle arrest and apoptosis of thyroid cancer cells [7]. We aimed to explore the therapeutic potential of novel galectin-3 inhibitors in thyroid cancer
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