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- Publisher Website: 10.1016/j.biopha.2024.116269
- Scopus: eid_2-s2.0-85186740509
- PMID: 38367549
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Article: Anti-metastatic effects of AGS-30 on breast cancer through the inhibition of M2-like macrophage polarization
Title | Anti-metastatic effects of AGS-30 on breast cancer through the inhibition of M2-like macrophage polarization |
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Authors | |
Keywords | Andrographolide derivative Breast cancer Cancer metastasis. Macrophage polarization |
Issue Date | 16-Feb-2024 |
Publisher | Elsevier |
Citation | Biomedicine and Pharmacotherapy, 2024, v. 172 How to Cite? |
Abstract | AGS-30, a new andrographolide derivative, showed significant anticancer and anti-angiogenic characteristics. However, its role in controlling macrophage polarization and tumor immune response is unknown. Thus, the main goals of this study are to investigate how AGS-30 regulates macrophage polarization and how it suppresses breast cancer metastasis. AGS-30 inhibited IL-4 and IL-13-induced RAW 264.7 and THP-1 macrophages into M2-like phenotype. However, AGS-30 did not affect the LPS and IFN-γ-induced polarization of M1-like macrophages. AGS-30 reduced the mRNA expressions of CD206, Arg-1, Fizz-1, Ym-1, VEGF, IL-10, MMP2, and MMP9 in M2-like macrophages in a concentration-dependent manner. In contrast, andrographolide treatment at 5 μM did not affect M1-like and M2-like macrophage polarization. The conditioned medium from M2-like macrophages increased 4T1 breast cancer cell migration and invasion, whereas AGS-30 inhibited these effects. In the 4T1 breast tumor xenograft mice, the tumor volume and weight were reduced without affecting body weight after receiving AGS-30. AGS-30 treatment also reduced lung and liver metastasis, with reduced STAT6, CD31, VEGF, and Ki67 protein expressions. Moreover, the tumors had considerably fewer M2-like macrophages and Arg-1 expression, but the proportion of M1-like macrophages and iNOS expression increased after AGS-30 treatment. Same results were found in the tail vein metastasis model. In conclusion, this study shows that AGS-30 inhibits breast cancer growth and metastasis, probably through inhibiting M2-like macrophage polarization. Our findings suggest that AGS-30 may be a potential immunotherapeutic alternative for metastatic breast cancer. |
Persistent Identifier | http://hdl.handle.net/10722/346009 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 1.493 |
DC Field | Value | Language |
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dc.contributor.author | Li, Jingjing | - |
dc.contributor.author | Liu, Zhuyun | - |
dc.contributor.author | Wu, Xiaoping | - |
dc.contributor.author | Lee, Simon Ming Yuen | - |
dc.contributor.author | Seto, Sai Wang | - |
dc.contributor.author | Zhang, Jinming | - |
dc.contributor.author | Zhou, Guo Chun | - |
dc.contributor.author | Leung, George Pak Heng | - |
dc.date.accessioned | 2024-09-06T00:30:25Z | - |
dc.date.available | 2024-09-06T00:30:25Z | - |
dc.date.issued | 2024-02-16 | - |
dc.identifier.citation | Biomedicine and Pharmacotherapy, 2024, v. 172 | - |
dc.identifier.issn | 0753-3322 | - |
dc.identifier.uri | http://hdl.handle.net/10722/346009 | - |
dc.description.abstract | AGS-30, a new andrographolide derivative, showed significant anticancer and anti-angiogenic characteristics. However, its role in controlling macrophage polarization and tumor immune response is unknown. Thus, the main goals of this study are to investigate how AGS-30 regulates macrophage polarization and how it suppresses breast cancer metastasis. AGS-30 inhibited IL-4 and IL-13-induced RAW 264.7 and THP-1 macrophages into M2-like phenotype. However, AGS-30 did not affect the LPS and IFN-γ-induced polarization of M1-like macrophages. AGS-30 reduced the mRNA expressions of CD206, Arg-1, Fizz-1, Ym-1, VEGF, IL-10, MMP2, and MMP9 in M2-like macrophages in a concentration-dependent manner. In contrast, andrographolide treatment at 5 μM did not affect M1-like and M2-like macrophage polarization. The conditioned medium from M2-like macrophages increased 4T1 breast cancer cell migration and invasion, whereas AGS-30 inhibited these effects. In the 4T1 breast tumor xenograft mice, the tumor volume and weight were reduced without affecting body weight after receiving AGS-30. AGS-30 treatment also reduced lung and liver metastasis, with reduced STAT6, CD31, VEGF, and Ki67 protein expressions. Moreover, the tumors had considerably fewer M2-like macrophages and Arg-1 expression, but the proportion of M1-like macrophages and iNOS expression increased after AGS-30 treatment. Same results were found in the tail vein metastasis model. In conclusion, this study shows that AGS-30 inhibits breast cancer growth and metastasis, probably through inhibiting M2-like macrophage polarization. Our findings suggest that AGS-30 may be a potential immunotherapeutic alternative for metastatic breast cancer. | - |
dc.language | eng | - |
dc.publisher | Elsevier | - |
dc.relation.ispartof | Biomedicine and Pharmacotherapy | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | Andrographolide derivative | - |
dc.subject | Breast cancer | - |
dc.subject | Cancer metastasis. | - |
dc.subject | Macrophage polarization | - |
dc.title | Anti-metastatic effects of AGS-30 on breast cancer through the inhibition of M2-like macrophage polarization | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.biopha.2024.116269 | - |
dc.identifier.pmid | 38367549 | - |
dc.identifier.scopus | eid_2-s2.0-85186740509 | - |
dc.identifier.volume | 172 | - |
dc.identifier.eissn | 1950-6007 | - |
dc.identifier.issnl | 0753-3322 | - |