ArticleScientific reports2026
γ-Tocotrienol inhibition of galectin-3 expression, distribution and oligomerization in highly metastatic breast cancer cells.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Experimental studies were conducted to compare the relative effects of γ-tocotrienol, a natural isoform within the vitamin E family of compounds, with established galectin-3 inhibitor β-lactose, on galectin-3 levels and distribution in highly metastatic human MDA-MB-231, and mouse + SA and TS/A breast cancer cell lines. In contrast to β-lactose, γ-tocotrienol displays a dual-mode binding profile with the carbohydrate recognition domain and hydrophobic pocket located on galectin-3, as determined using Schrödinger molecular modeling. However, treatment with either γ-tocotrienol or β-lactose induces a significant decrease in galectin-3 expression, oligomerization, and a corresponding decrease in fibronectin fibril and lamellipodial protrusion formation, an indication of treatment-induced reversal in epithelial-mesenchymal transition (EMT). These same treatments also caused a significant decrease in galectin-3 Fluorescence Resonance Energy Transfer (FRET) signaling, as compared to the control group, demonstrating the intricate role of galectin-3 in modulating EMT in metastatic breast cancer cells. Combined treatment of doxorubicin with either γ-tocotrienol or β-lactose results in a large increase in doxorubicin levels in the nuclei of metastatic breast cancer cells, the primary site of action for this chemotherapeutic agent. Taken together these findings demonstrate that γ-tocotrienol-induced reversal of EMT in metastatic breast cancer cells is mediated, at least in part, by a disruption in the galectin-3 expression, distribution and function.
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