ArticleJournal of molecular histology2026
Astragaloside II suppresses colorectal cancer progression by upregulating LGALS4 expression.
Article in Journal of molecular histology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
This study investigates the inhibitory effect of astragaloside II (AGS-II) on colorectal cancer (CRC) progression and elucidates the underlying mechanism involving LGALS4. The effects of AGS-II on proliferation, migration, and apoptosis of CRC cells were assessed using cell counting kit-8, colony formation, scratch wound, and flow cytometry assays. Potential targets were screened through integrated bioinformatics analysis and validated via RT-qPCR and Western blot. Molecular docking and molecular dynamics simulation were performed to evaluate the direct interaction between AGS-II and LGALS4. Functional experiments were conducted using gene overexpression and RNA interference. An in vivo xenograft model was employed to assess therapeutic efficacy. AGS-II significantly inhibited CRC cell proliferation and migration while inducing apoptosis in a dose-dependent manner. Bioinformatics analysis and experimental validation identified LGALS4 as a key target of AGS-II, with its high expression correlating with favorable patient prognosis. Molecular docking revealed a favorable binding affinity (Vina score: -9.2 kcal/mol), and molecular dynamics simulation confirmed the stability of the AGS-II-LGALS4 complex over 100 ns. Functional assays demonstrated that LGALS4 overexpression suppressed malignant phenotypes, whereas LGALS4 knockdown reversed the antitumor effects of AGS-II. In vivo experiments confirmed that AGS-II inhibited tumor growth by upregulating LGALS4. AGS-II suppresses CRC progression by upregulating LGALS4 expression, providing a novel candidate target and therapeutic strategy for CRC.
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