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...
Gespeichert in:
Veröffentlicht in: | Functional & integrative genomics 2023-06, Vol.23 (2), p.133-133, Article 133 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 133 |
---|---|
container_issue | 2 |
container_start_page | 133 |
container_title | Functional & integrative genomics |
container_volume | 23 |
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. |
doi_str_mv | 10.1007/s10142-023-01017-z |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_3040483948</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2805029818</sourcerecordid><originalsourceid>FETCH-LOGICAL-c408t-b82b9973d9dc7cecdf4665035511aff3e720d6e5e2986d1e7530b6cbacc32eac3</originalsourceid><addsrcrecordid>eNqFkc1O3TAQha2qVaHQF-iistRNN-kd2_lxlggBRQJ10duKneXYTmKUxKmdIHFfpu_Ag_BMdQilUhew8tj-5ozOHIQ-EPhCAIpNIEBSmgBlCcSySHav0D5JGU-KMuWvn2p2tYfehXANABmU7C3aYwVwQoDvo99HYfKykZ0LVht8_hOHeRy9CcEEPLUG97bxcrJuwHLQ-ORyi0fvmgVY3lyNlfE3VskOKznEOt67LuDqFtuhtZWd7NDgXirvxlY2Bl9SPLpOertbVafWu7lp8fbs9P5u872Xmm4YDrYZZBdbD9GbWnbBvH88D9CP05Pt8dfk4tvZ-fHRRaJS4FNScVqVZcF0qVWhjNJ1mucZsCwjRNY1MwUFnZvM0JLnmpgiY1DlqpJKMWqkYgfo86ob3f2aTZhEb8NiRQ7GzUEwSCHlLO71RZTyuOY4hyzop__Qazf76OyBYnkJQLJI0ZWKSwrBm1qM3vbS3woCYklarEmLmLR4SFrsYtPHR-m56o1-avkbbQTYCoT4NTTG_5v9jOwflFa27g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2803690015</pqid></control><display><type>article</type><title>Astragaloside IV suppresses the migration and EMT progression of cervical cancer cells by inhibiting macrophage M2 polarization through TGFβ/Smad2/3 signaling</title><source>MEDLINE</source><source>SpringerLink (Online service)</source><creator>Shen, Ling ; Li, Yuancheng ; Hu, Guiying ; Song, Xinli ; Wang, Xiaoshuang ; Li, Xiaoqi ; Xu, Xiaoyuan</creator><creatorcontrib>Shen, Ling ; Li, Yuancheng ; Hu, Guiying ; Song, Xinli ; Wang, Xiaoshuang ; Li, Xiaoqi ; Xu, Xiaoyuan</creatorcontrib><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.</description><identifier>ISSN: 1438-793X</identifier><identifier>EISSN: 1438-7948</identifier><identifier>DOI: 10.1007/s10142-023-01017-z</identifier><identifier>PMID: 37081108</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>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</subject><ispartof>Functional & integrative genomics, 2023-06, Vol.23 (2), p.133-133, Article 133</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-b82b9973d9dc7cecdf4665035511aff3e720d6e5e2986d1e7530b6cbacc32eac3</citedby><cites>FETCH-LOGICAL-c408t-b82b9973d9dc7cecdf4665035511aff3e720d6e5e2986d1e7530b6cbacc32eac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10142-023-01017-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10142-023-01017-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37081108$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shen, Ling</creatorcontrib><creatorcontrib>Li, Yuancheng</creatorcontrib><creatorcontrib>Hu, Guiying</creatorcontrib><creatorcontrib>Song, Xinli</creatorcontrib><creatorcontrib>Wang, Xiaoshuang</creatorcontrib><creatorcontrib>Li, Xiaoqi</creatorcontrib><creatorcontrib>Xu, Xiaoyuan</creatorcontrib><title>Astragaloside IV suppresses the migration and EMT progression of cervical cancer cells by inhibiting macrophage M2 polarization through TGFβ/Smad2/3 signaling</title><title>Functional & integrative genomics</title><addtitle>Funct Integr Genomics</addtitle><addtitle>Funct Integr Genomics</addtitle><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.</description><subject>Angiogenesis</subject><subject>Animal Genetics and Genomics</subject><subject>antineoplastic activity</subject><subject>Antitumor activity</subject><subject>astragalosides</subject><subject>Biochemistry</subject><subject>Bioinformatics</subject><subject>Biomedical and Life Sciences</subject><subject>CD163 antigen</subject><subject>Cell Biology</subject><subject>cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cervical cancer</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Female</subject><subject>flow cytometry</subject><subject>genomics</subject><subject>Gynecological cancer</subject><subject>Humans</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-10 - metabolism</subject><subject>Interleukin-10 - pharmacology</subject><subject>Leukocyte migration</subject><subject>Life Sciences</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Microbial Genetics and Genomics</subject><subject>migratory behavior</subject><subject>neoplasm cells</subject><subject>Original Article</subject><subject>Plant Genetics and Genomics</subject><subject>protein synthesis</subject><subject>Smad2 Protein - genetics</subject><subject>Smad2 Protein - metabolism</subject><subject>Smad2 Protein - pharmacology</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming growth factor-b</subject><subject>uterine cervical neoplasms</subject><subject>Uterine Cervical Neoplasms - drug therapy</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Wound healing</subject><issn>1438-793X</issn><issn>1438-7948</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkc1O3TAQha2qVaHQF-iistRNN-kd2_lxlggBRQJ10duKneXYTmKUxKmdIHFfpu_Ag_BMdQilUhew8tj-5ozOHIQ-EPhCAIpNIEBSmgBlCcSySHav0D5JGU-KMuWvn2p2tYfehXANABmU7C3aYwVwQoDvo99HYfKykZ0LVht8_hOHeRy9CcEEPLUG97bxcrJuwHLQ-ORyi0fvmgVY3lyNlfE3VskOKznEOt67LuDqFtuhtZWd7NDgXirvxlY2Bl9SPLpOertbVafWu7lp8fbs9P5u872Xmm4YDrYZZBdbD9GbWnbBvH88D9CP05Pt8dfk4tvZ-fHRRaJS4FNScVqVZcF0qVWhjNJ1mucZsCwjRNY1MwUFnZvM0JLnmpgiY1DlqpJKMWqkYgfo86ob3f2aTZhEb8NiRQ7GzUEwSCHlLO71RZTyuOY4hyzop__Qazf76OyBYnkJQLJI0ZWKSwrBm1qM3vbS3woCYklarEmLmLR4SFrsYtPHR-m56o1-avkbbQTYCoT4NTTG_5v9jOwflFa27g</recordid><startdate>20230601</startdate><enddate>20230601</enddate><creator>Shen, Ling</creator><creator>Li, Yuancheng</creator><creator>Hu, Guiying</creator><creator>Song, Xinli</creator><creator>Wang, Xiaoshuang</creator><creator>Li, Xiaoqi</creator><creator>Xu, Xiaoyuan</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PADUT</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>20230601</creationdate><title>Astragaloside IV suppresses the migration and EMT progression of cervical cancer cells by inhibiting macrophage M2 polarization through TGFβ/Smad2/3 signaling</title><author>Shen, Ling ; Li, Yuancheng ; Hu, Guiying ; Song, Xinli ; Wang, Xiaoshuang ; Li, Xiaoqi ; Xu, Xiaoyuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-b82b9973d9dc7cecdf4665035511aff3e720d6e5e2986d1e7530b6cbacc32eac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Angiogenesis</topic><topic>Animal Genetics and Genomics</topic><topic>antineoplastic activity</topic><topic>Antitumor activity</topic><topic>astragalosides</topic><topic>Biochemistry</topic><topic>Bioinformatics</topic><topic>Biomedical and Life Sciences</topic><topic>CD163 antigen</topic><topic>Cell Biology</topic><topic>cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cervical cancer</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Female</topic><topic>flow cytometry</topic><topic>genomics</topic><topic>Gynecological cancer</topic><topic>Humans</topic><topic>Interleukin 10</topic><topic>Interleukin-10 - genetics</topic><topic>Interleukin-10 - metabolism</topic><topic>Interleukin-10 - pharmacology</topic><topic>Leukocyte migration</topic><topic>Life Sciences</topic><topic>Macrophages</topic><topic>Macrophages - metabolism</topic><topic>Microbial Genetics and Genomics</topic><topic>migratory behavior</topic><topic>neoplasm cells</topic><topic>Original Article</topic><topic>Plant Genetics and Genomics</topic><topic>protein synthesis</topic><topic>Smad2 Protein - genetics</topic><topic>Smad2 Protein - metabolism</topic><topic>Smad2 Protein - pharmacology</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Transforming growth factor-b</topic><topic>uterine cervical neoplasms</topic><topic>Uterine Cervical Neoplasms - drug therapy</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shen, Ling</creatorcontrib><creatorcontrib>Li, Yuancheng</creatorcontrib><creatorcontrib>Hu, Guiying</creatorcontrib><creatorcontrib>Song, Xinli</creatorcontrib><creatorcontrib>Wang, Xiaoshuang</creatorcontrib><creatorcontrib>Li, Xiaoqi</creatorcontrib><creatorcontrib>Xu, Xiaoyuan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (Proquest)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest research library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Research Library China</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Functional & integrative genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shen, Ling</au><au>Li, Yuancheng</au><au>Hu, Guiying</au><au>Song, Xinli</au><au>Wang, Xiaoshuang</au><au>Li, Xiaoqi</au><au>Xu, Xiaoyuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astragaloside IV suppresses the migration and EMT progression of cervical cancer cells by inhibiting macrophage M2 polarization through TGFβ/Smad2/3 signaling</atitle><jtitle>Functional & 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> |
fulltext | fulltext |
identifier | ISSN: 1438-793X |
ispartof | Functional & integrative genomics, 2023-06, Vol.23 (2), p.133-133, Article 133 |
issn | 1438-793X 1438-7948 |
language | eng |
recordid | cdi_proquest_miscellaneous_3040483948 |
source | MEDLINE; SpringerLink (Online service) |
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 |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-12T01%3A14%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Astragaloside%20IV%20suppresses%20the%20migration%20and%20EMT%20progression%20of%20cervical%20cancer%20cells%20by%20inhibiting%20macrophage%20M2%20polarization%20through%20TGF%CE%B2/Smad2/3%20signaling&rft.jtitle=Functional%20&%20integrative%20genomics&rft.au=Shen,%20Ling&rft.date=2023-06-01&rft.volume=23&rft.issue=2&rft.spage=133&rft.epage=133&rft.pages=133-133&rft.artnum=133&rft.issn=1438-793X&rft.eissn=1438-7948&rft_id=info:doi/10.1007/s10142-023-01017-z&rft_dat=%3Cproquest_cross%3E2805029818%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2803690015&rft_id=info:pmid/37081108&rfr_iscdi=true |