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<p>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.</p>

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Astragaloside II suppresses colorectal cancer progression by upregulating LGALS4 expression

  • 期刊论文

  • 发表日期：

    2026年6月29日

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  • Yingying Su,
  • Dan Lu,
  • Rongqiang Zhang,
  • Zhiyong Shao

摘要

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.