Macrophages-stimulated PRMT1-mediated EZH2 methylation promotes breast cancer metastasis
Tumor-associated macrophages (TAMs) are important monocytes in the breast cancer microenvironment. They facilitate the distant metastasis of breast cancer. However, the detailed mechanisms of TAM-derived cancer metastasis have not been clearly elucidated. Here, we demonstrate that PRMT1 is essential...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2020-12, Vol.533 (4), p.679-684 |
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| creator | Li, Zhongwei Wang, Diandian Wang, Wenwen Chen, Xintian Tang, Anqun Hou, Pingfu Li, Minle Zheng, Junnian Bai, Jin |
| description | Tumor-associated macrophages (TAMs) are important monocytes in the breast cancer microenvironment. They facilitate the distant metastasis of breast cancer. However, the detailed mechanisms of TAM-derived cancer metastasis have not been clearly elucidated. Here, we demonstrate that PRMT1 is essential for TAM-mediated breast cancer cell migration and metastasis. TAMs increase EZH2 stability by stimulating PRMT1-mediated meR342-EZH2 formation through the secretion of interleukin-6 (IL-6) cytokine. Moreover, high expression levels of TAMs are positively correlated with PRMT1, meR342-EZH2, and EZH2 expression in breast cancer patients. Our study presents a novel mechanism of TAM-induced breast cancer metastasis via the IL-6-PRMT1-meR342-EZH2 axis.
•PRMT1 is required for TAMs-mediated breast cancer metastasis.•TAMs stimulate PRMT1 expression by secreting IL-6.•TAMs promote breast cancer metastasis through IL-6-PRMT1-CDK1-TRAF6-EZH2 axis.•CD163 (a TAMs marker) is positive correlated with PRMT1, meR342-EZH2 and EZH2 expression in breast cancer samples. |
| doi_str_mv | 10.1016/j.bbrc.2020.10.037 |
| format | Article |
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•PRMT1 is required for TAMs-mediated breast cancer metastasis.•TAMs stimulate PRMT1 expression by secreting IL-6.•TAMs promote breast cancer metastasis through IL-6-PRMT1-CDK1-TRAF6-EZH2 axis.•CD163 (a TAMs marker) is positive correlated with PRMT1, meR342-EZH2 and EZH2 expression in breast cancer samples.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2020.10.037</identifier><identifier>PMID: 33092789</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer metastasis ; Cell Line, Tumor ; Cell Movement - genetics ; Enhancer of Zeste Homolog 2 Protein - metabolism ; EZH2 ; Female ; Gene Expression Regulation, Neoplastic - genetics ; Humans ; IL-6 ; Immunohistochemistry ; Interleukin-6 - metabolism ; Intracellular Signaling Peptides and Proteins - metabolism ; Macrophages - metabolism ; Methylation ; Mice ; Mice, Inbred BALB C ; Neoplasm Metastasis ; Post-translational modifications ; PRMT1 ; Protein Stability ; Protein-Arginine N-Methyltransferases - genetics ; Protein-Arginine N-Methyltransferases - metabolism ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Tumor Microenvironment - genetics ; Tumor-associated macrophages ; Ubiquitination ; Xenograft Model Antitumor Assays</subject><ispartof>Biochemical and biophysical research communications, 2020-12, Vol.533 (4), p.679-684</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-4acf03ef3d4bf7d6bd6959872a5f730e386574f7c3c94733e85cf1f66bb6c7c33</citedby><cites>FETCH-LOGICAL-c356t-4acf03ef3d4bf7d6bd6959872a5f730e386574f7c3c94733e85cf1f66bb6c7c33</cites><orcidid>0000-0003-0208-6410</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2020.10.037$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33092789$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Zhongwei</creatorcontrib><creatorcontrib>Wang, Diandian</creatorcontrib><creatorcontrib>Wang, Wenwen</creatorcontrib><creatorcontrib>Chen, Xintian</creatorcontrib><creatorcontrib>Tang, Anqun</creatorcontrib><creatorcontrib>Hou, Pingfu</creatorcontrib><creatorcontrib>Li, Minle</creatorcontrib><creatorcontrib>Zheng, Junnian</creatorcontrib><creatorcontrib>Bai, Jin</creatorcontrib><title>Macrophages-stimulated PRMT1-mediated EZH2 methylation promotes breast cancer metastasis</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Tumor-associated macrophages (TAMs) are important monocytes in the breast cancer microenvironment. They facilitate the distant metastasis of breast cancer. However, the detailed mechanisms of TAM-derived cancer metastasis have not been clearly elucidated. Here, we demonstrate that PRMT1 is essential for TAM-mediated breast cancer cell migration and metastasis. TAMs increase EZH2 stability by stimulating PRMT1-mediated meR342-EZH2 formation through the secretion of interleukin-6 (IL-6) cytokine. Moreover, high expression levels of TAMs are positively correlated with PRMT1, meR342-EZH2, and EZH2 expression in breast cancer patients. Our study presents a novel mechanism of TAM-induced breast cancer metastasis via the IL-6-PRMT1-meR342-EZH2 axis.
•PRMT1 is required for TAMs-mediated breast cancer metastasis.•TAMs stimulate PRMT1 expression by secreting IL-6.•TAMs promote breast cancer metastasis through IL-6-PRMT1-CDK1-TRAF6-EZH2 axis.•CD163 (a TAMs marker) is positive correlated with PRMT1, meR342-EZH2 and EZH2 expression in breast cancer samples.</description><subject>Animals</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer metastasis</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Enhancer of Zeste Homolog 2 Protein - metabolism</subject><subject>EZH2</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Humans</subject><subject>IL-6</subject><subject>Immunohistochemistry</subject><subject>Interleukin-6 - metabolism</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Macrophages - metabolism</subject><subject>Methylation</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Neoplasm Metastasis</subject><subject>Post-translational modifications</subject><subject>PRMT1</subject><subject>Protein Stability</subject><subject>Protein-Arginine N-Methyltransferases - genetics</subject><subject>Protein-Arginine N-Methyltransferases - metabolism</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Tumor Microenvironment - genetics</subject><subject>Tumor-associated macrophages</subject><subject>Ubiquitination</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEFLAzEQhYMotlb_gAfZo5etk2Q32wUvUqoVWhSpULyEbHZiU7rdmuwK_fdmrXr0NMybN4-Zj5BLCkMKVNysh0Xh9JAB64Qh8OyI9CnkEDMKyTHpA4CIWU6XPXLm_RqA0kTkp6THOeQsG-V9spwr7erdSr2jj31jq3ajGiyj55f5gsYVlva7nbxNWVRhs9qHsa230c7VVd2gjwqHyjeRVluNrrOETnnrz8mJURuPFz91QF7vJ4vxNJ49PTyO72ax5qlo4kRpAxwNL5PCZKUoSpGn-ShjKjUZB-QjkWaJyTTXeZJxjqNUG2qEKAqhg8oH5PqQGy76aNE3srJe42ajtli3XrIkTQINEBCs7GANH3vv0Mids5Vye0lBdkTlWnZEZUe00wLRsHT1k98WAcffyi_CYLg9GDB8-WnRSa8tBhqldagbWdb2v_wvq7iH2A</recordid><startdate>20201217</startdate><enddate>20201217</enddate><creator>Li, Zhongwei</creator><creator>Wang, Diandian</creator><creator>Wang, Wenwen</creator><creator>Chen, Xintian</creator><creator>Tang, Anqun</creator><creator>Hou, Pingfu</creator><creator>Li, Minle</creator><creator>Zheng, Junnian</creator><creator>Bai, Jin</creator><general>Elsevier Inc</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>7X8</scope><orcidid>https://orcid.org/0000-0003-0208-6410</orcidid></search><sort><creationdate>20201217</creationdate><title>Macrophages-stimulated PRMT1-mediated EZH2 methylation promotes breast cancer metastasis</title><author>Li, Zhongwei ; Wang, Diandian ; Wang, Wenwen ; Chen, Xintian ; Tang, Anqun ; Hou, Pingfu ; Li, Minle ; Zheng, Junnian ; Bai, Jin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-4acf03ef3d4bf7d6bd6959872a5f730e386574f7c3c94733e85cf1f66bb6c7c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer metastasis</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Enhancer of Zeste Homolog 2 Protein - metabolism</topic><topic>EZH2</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Humans</topic><topic>IL-6</topic><topic>Immunohistochemistry</topic><topic>Interleukin-6 - metabolism</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Macrophages - metabolism</topic><topic>Methylation</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Neoplasm Metastasis</topic><topic>Post-translational modifications</topic><topic>PRMT1</topic><topic>Protein Stability</topic><topic>Protein-Arginine N-Methyltransferases - genetics</topic><topic>Protein-Arginine N-Methyltransferases - metabolism</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Tumor Microenvironment - genetics</topic><topic>Tumor-associated macrophages</topic><topic>Ubiquitination</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Zhongwei</creatorcontrib><creatorcontrib>Wang, Diandian</creatorcontrib><creatorcontrib>Wang, Wenwen</creatorcontrib><creatorcontrib>Chen, Xintian</creatorcontrib><creatorcontrib>Tang, Anqun</creatorcontrib><creatorcontrib>Hou, Pingfu</creatorcontrib><creatorcontrib>Li, Minle</creatorcontrib><creatorcontrib>Zheng, Junnian</creatorcontrib><creatorcontrib>Bai, Jin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Zhongwei</au><au>Wang, Diandian</au><au>Wang, Wenwen</au><au>Chen, Xintian</au><au>Tang, Anqun</au><au>Hou, Pingfu</au><au>Li, Minle</au><au>Zheng, Junnian</au><au>Bai, Jin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Macrophages-stimulated PRMT1-mediated EZH2 methylation promotes breast cancer metastasis</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2020-12-17</date><risdate>2020</risdate><volume>533</volume><issue>4</issue><spage>679</spage><epage>684</epage><pages>679-684</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Tumor-associated macrophages (TAMs) are important monocytes in the breast cancer microenvironment. They facilitate the distant metastasis of breast cancer. However, the detailed mechanisms of TAM-derived cancer metastasis have not been clearly elucidated. Here, we demonstrate that PRMT1 is essential for TAM-mediated breast cancer cell migration and metastasis. TAMs increase EZH2 stability by stimulating PRMT1-mediated meR342-EZH2 formation through the secretion of interleukin-6 (IL-6) cytokine. Moreover, high expression levels of TAMs are positively correlated with PRMT1, meR342-EZH2, and EZH2 expression in breast cancer patients. Our study presents a novel mechanism of TAM-induced breast cancer metastasis via the IL-6-PRMT1-meR342-EZH2 axis.
•PRMT1 is required for TAMs-mediated breast cancer metastasis.•TAMs stimulate PRMT1 expression by secreting IL-6.•TAMs promote breast cancer metastasis through IL-6-PRMT1-CDK1-TRAF6-EZH2 axis.•CD163 (a TAMs marker) is positive correlated with PRMT1, meR342-EZH2 and EZH2 expression in breast cancer samples.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>33092789</pmid><doi>10.1016/j.bbrc.2020.10.037</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0003-0208-6410</orcidid></addata></record> |
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| subjects | Animals Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer metastasis Cell Line, Tumor Cell Movement - genetics Enhancer of Zeste Homolog 2 Protein - metabolism EZH2 Female Gene Expression Regulation, Neoplastic - genetics Humans IL-6 Immunohistochemistry Interleukin-6 - metabolism Intracellular Signaling Peptides and Proteins - metabolism Macrophages - metabolism Methylation Mice Mice, Inbred BALB C Neoplasm Metastasis Post-translational modifications PRMT1 Protein Stability Protein-Arginine N-Methyltransferases - genetics Protein-Arginine N-Methyltransferases - metabolism Repressor Proteins - genetics Repressor Proteins - metabolism Tumor Microenvironment - genetics Tumor-associated macrophages Ubiquitination Xenograft Model Antitumor Assays |
| title | Macrophages-stimulated PRMT1-mediated EZH2 methylation promotes breast cancer metastasis |
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