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Complement Component 3 Is Regulated by TWIST1 and Mediates Epithelial-Mesenchymal Transition
We have previously shown that complement component 3 (C3) is secreted by malignant epithelial cells. To understand the mechanism of upregulation of C3 expression in tumor cells, we studied the C3 promoter and identified that twist basic helix-loop-helix transcription factor 1 (TWIST1) binds to the C...
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Published in: | The Journal of immunology (1950) 2016-02, Vol.196 (3), p.1412-1418 |
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container_issue | 3 |
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container_title | The Journal of immunology (1950) |
container_volume | 196 |
creator | Cho, Min Soon Rupaimoole, Rajesha Choi, Hyun-Jin Noh, Kyunghee Chen, Jichao Hu, Qianghua Sood, Anil K Afshar-Kharghan, Vahid |
description | We have previously shown that complement component 3 (C3) is secreted by malignant epithelial cells. To understand the mechanism of upregulation of C3 expression in tumor cells, we studied the C3 promoter and identified that twist basic helix-loop-helix transcription factor 1 (TWIST1) binds to the C3 promoter and enhances its expression. Because TWIST1 mediates epithelial-mesenchymal transition (EMT), we studied the effect of C3 on EMT and found that C3 decreased E-cadherin expression on cancer cells and promoted EMT. We showed that C3-induced reduction in E-cadherin expression in ovarian cancer cells was mediated by C3a and is Krüppel-like factor 5 dependent. We investigated the association between TWIST1 and C3 in malignant tumors and in murine embryos. TWIST1 and C3 colocalized at the invasive tumor edges, and in the neural crest and limb buds of mouse embryos. Our results identified TWIST1 as a transcription factor that regulates C3 expression during pathologic and physiologic EMT. |
doi_str_mv | 10.4049/jimmunol.1501886 |
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To understand the mechanism of upregulation of C3 expression in tumor cells, we studied the C3 promoter and identified that twist basic helix-loop-helix transcription factor 1 (TWIST1) binds to the C3 promoter and enhances its expression. Because TWIST1 mediates epithelial-mesenchymal transition (EMT), we studied the effect of C3 on EMT and found that C3 decreased E-cadherin expression on cancer cells and promoted EMT. We showed that C3-induced reduction in E-cadherin expression in ovarian cancer cells was mediated by C3a and is Krüppel-like factor 5 dependent. We investigated the association between TWIST1 and C3 in malignant tumors and in murine embryos. TWIST1 and C3 colocalized at the invasive tumor edges, and in the neural crest and limb buds of mouse embryos. Our results identified TWIST1 as a transcription factor that regulates C3 expression during pathologic and physiologic EMT.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1501886</identifier><identifier>PMID: 26718342</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Blotting, Western ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; Complement C3 - biosynthesis ; Complement C3 - genetics ; Epithelial-Mesenchymal Transition - physiology ; Female ; Gene Expression Regulation, Neoplastic - physiology ; Humans ; Immunohistochemistry ; Mice ; Mutagenesis, Site-Directed ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Real-Time Polymerase Chain Reaction ; RNA, Small Interfering ; Transfection ; Twist-Related Protein 1 - genetics ; Twist-Related Protein 1 - metabolism</subject><ispartof>The Journal of immunology (1950), 2016-02, Vol.196 (3), p.1412-1418</ispartof><rights>Copyright © 2016 by The American Association of Immunologists, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-e63bc51bb4b8c10ab5a3ef1ac410e2cc215b44e83d3ee6358cd60af77c2fb5853</citedby><cites>FETCH-LOGICAL-c462t-e63bc51bb4b8c10ab5a3ef1ac410e2cc215b44e83d3ee6358cd60af77c2fb5853</cites><orcidid>0000-0003-2749-8550 ; 0000-0002-9992-8356</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26718342$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cho, Min Soon</creatorcontrib><creatorcontrib>Rupaimoole, Rajesha</creatorcontrib><creatorcontrib>Choi, Hyun-Jin</creatorcontrib><creatorcontrib>Noh, Kyunghee</creatorcontrib><creatorcontrib>Chen, Jichao</creatorcontrib><creatorcontrib>Hu, Qianghua</creatorcontrib><creatorcontrib>Sood, Anil K</creatorcontrib><creatorcontrib>Afshar-Kharghan, Vahid</creatorcontrib><title>Complement Component 3 Is Regulated by TWIST1 and Mediates Epithelial-Mesenchymal Transition</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>We have previously shown that complement component 3 (C3) is secreted by malignant epithelial cells. To understand the mechanism of upregulation of C3 expression in tumor cells, we studied the C3 promoter and identified that twist basic helix-loop-helix transcription factor 1 (TWIST1) binds to the C3 promoter and enhances its expression. Because TWIST1 mediates epithelial-mesenchymal transition (EMT), we studied the effect of C3 on EMT and found that C3 decreased E-cadherin expression on cancer cells and promoted EMT. We showed that C3-induced reduction in E-cadherin expression in ovarian cancer cells was mediated by C3a and is Krüppel-like factor 5 dependent. We investigated the association between TWIST1 and C3 in malignant tumors and in murine embryos. TWIST1 and C3 colocalized at the invasive tumor edges, and in the neural crest and limb buds of mouse embryos. Our results identified TWIST1 as a transcription factor that regulates C3 expression during pathologic and physiologic EMT.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cell Line, Tumor</subject><subject>Chromatin Immunoprecipitation</subject><subject>Complement C3 - biosynthesis</subject><subject>Complement C3 - genetics</subject><subject>Epithelial-Mesenchymal Transition - physiology</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Mice</subject><subject>Mutagenesis, Site-Directed</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>RNA, Small Interfering</subject><subject>Transfection</subject><subject>Twist-Related Protein 1 - genetics</subject><subject>Twist-Related Protein 1 - metabolism</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNpVUU1r3DAQFaWh2SS991R07MXp6NPOpVCWfCwkFNoNvRSEJI-zCrK0tezA_vt4ySa0p3nMvHnz8Qj5xOBcgrz4-hj6fko5njMFrGn0O7JgSkGlNej3ZAHAecVqXR-Tk1IeAUADlx_IMdc1a4TkC_JnmfttxB7TSPcwpz0SdFXoT3yYoh2xpW5H179Xv9aM2tTSO2zDnC70chvGDcZgY3WHBZPf7Hob6XqwqYQx5HRGjjobC348xFNyf3W5Xt5Utz-uV8vvt5WXmo8VauG8Ys5J13gG1ikrsGPWSwbIvedMOSmxEa3Amasa32qwXV173jnVKHFKvr3obifXY-vnEwYbzXYIvR12Jttg_q-ksDEP-cnImksl6lngy0FgyH8nLKPpQ_EYo02Yp2LmH8IFY0KJmQovVD_kUgbs3sYwMHtTzKsp5mDK3PL53_XeGl5dEM_SE4xC</recordid><startdate>20160201</startdate><enddate>20160201</enddate><creator>Cho, Min Soon</creator><creator>Rupaimoole, Rajesha</creator><creator>Choi, Hyun-Jin</creator><creator>Noh, Kyunghee</creator><creator>Chen, Jichao</creator><creator>Hu, Qianghua</creator><creator>Sood, Anil K</creator><creator>Afshar-Kharghan, Vahid</creator><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><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2749-8550</orcidid><orcidid>https://orcid.org/0000-0002-9992-8356</orcidid></search><sort><creationdate>20160201</creationdate><title>Complement Component 3 Is Regulated by TWIST1 and Mediates Epithelial-Mesenchymal Transition</title><author>Cho, Min Soon ; Rupaimoole, Rajesha ; Choi, Hyun-Jin ; Noh, Kyunghee ; Chen, Jichao ; Hu, Qianghua ; Sood, Anil K ; Afshar-Kharghan, Vahid</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-e63bc51bb4b8c10ab5a3ef1ac410e2cc215b44e83d3ee6358cd60af77c2fb5853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Blotting, Western</topic><topic>Cell Line, Tumor</topic><topic>Chromatin Immunoprecipitation</topic><topic>Complement C3 - biosynthesis</topic><topic>Complement C3 - genetics</topic><topic>Epithelial-Mesenchymal Transition - physiology</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Mice</topic><topic>Mutagenesis, Site-Directed</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>RNA, Small Interfering</topic><topic>Transfection</topic><topic>Twist-Related Protein 1 - genetics</topic><topic>Twist-Related Protein 1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cho, Min Soon</creatorcontrib><creatorcontrib>Rupaimoole, Rajesha</creatorcontrib><creatorcontrib>Choi, Hyun-Jin</creatorcontrib><creatorcontrib>Noh, Kyunghee</creatorcontrib><creatorcontrib>Chen, Jichao</creatorcontrib><creatorcontrib>Hu, Qianghua</creatorcontrib><creatorcontrib>Sood, Anil K</creatorcontrib><creatorcontrib>Afshar-Kharghan, Vahid</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cho, Min Soon</au><au>Rupaimoole, Rajesha</au><au>Choi, Hyun-Jin</au><au>Noh, Kyunghee</au><au>Chen, Jichao</au><au>Hu, Qianghua</au><au>Sood, Anil K</au><au>Afshar-Kharghan, Vahid</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Complement Component 3 Is Regulated by TWIST1 and Mediates Epithelial-Mesenchymal Transition</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>196</volume><issue>3</issue><spage>1412</spage><epage>1418</epage><pages>1412-1418</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>We have previously shown that complement component 3 (C3) is secreted by malignant epithelial cells. To understand the mechanism of upregulation of C3 expression in tumor cells, we studied the C3 promoter and identified that twist basic helix-loop-helix transcription factor 1 (TWIST1) binds to the C3 promoter and enhances its expression. Because TWIST1 mediates epithelial-mesenchymal transition (EMT), we studied the effect of C3 on EMT and found that C3 decreased E-cadherin expression on cancer cells and promoted EMT. We showed that C3-induced reduction in E-cadherin expression in ovarian cancer cells was mediated by C3a and is Krüppel-like factor 5 dependent. We investigated the association between TWIST1 and C3 in malignant tumors and in murine embryos. TWIST1 and C3 colocalized at the invasive tumor edges, and in the neural crest and limb buds of mouse embryos. 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subjects | Animals Blotting, Western Cell Line, Tumor Chromatin Immunoprecipitation Complement C3 - biosynthesis Complement C3 - genetics Epithelial-Mesenchymal Transition - physiology Female Gene Expression Regulation, Neoplastic - physiology Humans Immunohistochemistry Mice Mutagenesis, Site-Directed Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Nuclear Proteins - genetics Nuclear Proteins - metabolism Real-Time Polymerase Chain Reaction RNA, Small Interfering Transfection Twist-Related Protein 1 - genetics Twist-Related Protein 1 - metabolism |
title | Complement Component 3 Is Regulated by TWIST1 and Mediates Epithelial-Mesenchymal Transition |
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