Astragaloside IV suppresses the migration and EMT progression of cervical cancer cells by inhibiting macrophage M2 polarization through TGFβ/Smad2/3 signaling

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. T...

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Veröffentlicht in:Functional & integrative genomics 2023-06, Vol.23 (2), p.133-133, Article 133
Hauptverfasser: Shen, Ling, Li, Yuancheng, Hu, Guiying, Song, Xinli, Wang, Xiaoshuang, Li, Xiaoqi, Xu, Xiaoyuan
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container_start_page 133
container_title Functional & integrative genomics
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creator Shen, Ling
Li, Yuancheng
Hu, Guiying
Song, Xinli
Wang, Xiaoshuang
Li, Xiaoqi
Xu, Xiaoyuan
description 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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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. 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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. 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integrative genomics</jtitle><stitle>Funct Integr Genomics</stitle><addtitle>Funct Integr Genomics</addtitle><date>2023-06-01</date><risdate>2023</risdate><volume>23</volume><issue>2</issue><spage>133</spage><epage>133</epage><pages>133-133</pages><artnum>133</artnum><issn>1438-793X</issn><eissn>1438-7948</eissn><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.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>37081108</pmid><doi>10.1007/s10142-023-01017-z</doi><tpages>1</tpages></addata></record>
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subjects Angiogenesis
Animal Genetics and Genomics
antineoplastic activity
Antitumor activity
astragalosides
Biochemistry
Bioinformatics
Biomedical and Life Sciences
CD163 antigen
Cell Biology
cell growth
Cell Line, Tumor
Cervical cancer
Enzyme-linked immunosorbent assay
Epithelial-Mesenchymal Transition
Female
flow cytometry
genomics
Gynecological cancer
Humans
Interleukin 10
Interleukin-10 - genetics
Interleukin-10 - metabolism
Interleukin-10 - pharmacology
Leukocyte migration
Life Sciences
Macrophages
Macrophages - metabolism
Microbial Genetics and Genomics
migratory behavior
neoplasm cells
Original Article
Plant Genetics and Genomics
protein synthesis
Smad2 Protein - genetics
Smad2 Protein - metabolism
Smad2 Protein - pharmacology
Transforming Growth Factor beta - genetics
Transforming Growth Factor beta - metabolism
Transforming growth factor-b
uterine cervical neoplasms
Uterine Cervical Neoplasms - drug therapy
Uterine Cervical Neoplasms - genetics
Wound healing
title Astragaloside IV suppresses the migration and EMT progression of cervical cancer cells by inhibiting macrophage M2 polarization through TGFβ/Smad2/3 signaling
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