ArticleFunctional & integrative genomics2023
Astragaloside IV suppresses the migration and EMT progression of cervical cancer cells by inhibiting macrophage M2 polarization through TGFβ/Smad2/3 signaling.
Article in Functional & integrative genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Molecular mechanisms of astragaloside-IV in hepatocellular carcinoma therapy: a systematic review.BMC cancer · 2025Pooled it
- Mechanistic insights into the roles of astragalosides andOncology reports · 2026Review
- Advancement ofChinese herbal medicines · 2026Review
- Targeting macrophage polarization: mechanisms and potential of mesenchymal stromal/stem cells therapy in acne treatment- a narrative review.Frontiers in immunology · 2026Review
- Dynamic remodeling of the tumor immune microenvironment: immunometabolic regulatory networks of astragalus polysaccharides and astragaloside IV.Frontiers in pharmacology · 2026Review
- Berberine suppresses hepatocellular carcinoma progression by blocking IL-4-JAK1-STAT6-mediated M2 polarization of macrophage.Frontiers in pharmacology · 2025Article
- Macrophage polarization in disease therapy: insights from astragaloside IV and cycloastragenol.Frontiers in pharmacology · 2025Review
- Astragaloside IV: a potential nemesis for gastric cancer.Frontiers in pharmacology · 2025Review
- Astragaloside IV augments anti-PD-1 therapy to suppress tumor growth in lung cancer by remodeling the tumor microenvironment.European journal of histochemistry : EJH · 2024Article
- Extracellular vesicles and macrophages in tumor microenvironment: Impact on cervical cancer.Heliyon · 2024Review
- Epithelial-mesenchymal plasticity in cancer: signaling pathways and therapeutic targets.MedComm · 2024Review
- Research Progress on the Anti-Cancer Effects ofMolecules (Basel, Switzerland) · 2024Review
- Article
- The role and research progress of tumor-associated macrophages in cervical cancer.American journal of cancer research · 2024Review
- Isoliensinine suppressed gastric cancer cell proliferation and migration by targeting TGFBR1 to regulate TGF-β-smad signaling pathways.Frontiers in pharmacology · 2024Article
- Astragaloside IV enhances the sensitivity of breast cancer stem cells to paclitaxel by inhibiting stemness.Translational cancer research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Cervical cancer (CC) is a gynecological malignant tumor worldwide. Astragaloside IV (AS-IV) has been found to exert antitumor effects on CC. In addition, M2-polarized macrophages, known as tumor-associated macrophages (TAMs), play an important role in promoting cancer cell growth and angiogenesis. Thus, we explored the association between the antitumor effect of AS-IV and macrophage polarization in CC. Flow cytometry, ELISA, and RT‒qPCR assays were applied to detect the levels of CD163, IL-10, TGFβ, and CD206 in M2 macrophages with or without AS-IV treatment. In addition, conditioned medium (CM) was collected from these M2 macrophages, and CC cells were then cultured in various CMs. Wound healing and transwell assays were used to assess the migratory ability of CC cells. In this study, we found that AS-IV significantly inhibited M2 polarization of macrophages, as shown by decreased CD163, IL-10, TGFβ, and CD206 expression. In addition, compared with CM from M2 macrophages, CM from AS-IV-treated M2 macrophages notably inhibited angiogenesis, migration, and epithelial-mesenchymal transition (EMT) in CC cells. Furthermore, compared with CM from M2 macrophages, CM from AS-IV-treated M2 macrophages markedly reduced p-Smad2 and p-Smad3 protein expression in CC cells, and these changes were reversed by TGF-β treatment. Collectively, suppression of M2-like polarization of macrophages by AS-IV could prevent the migration and EMT of CC cells by inactivating TGF-β/Smad2/3 signaling. These findings might provide some theoretical support for exploring novel treatments for CC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.