Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133+ Ovarian Cancer Stem-Like Cells via NF-κB-Mediated MMP-9 Upregulation
The concept of cancer stem cells (CSCs) proposes that solely CSCs are capable of generating tumor metastases. However, how CSCs maintain their invasion and migration abilities, the most important properties of metastatic cells, still remains elusive. Here we used CD133 to mark a specific population...
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| Veröffentlicht in: | Stem cells (Dayton, Ohio) Ohio), 2012-10, Vol.30 (10), p.2309-2319 |
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| creator | Long, Haixia Xie, Rongkai Xiang, Tong Zhao, Zhongquan Lin, Sheng Liang, Zhiqing Chen, Zhengtang Zhu, Bo |
| description | The concept of cancer stem cells (CSCs) proposes that solely CSCs are capable of generating tumor metastases. However, how CSCs maintain their invasion and migration abilities, the most important properties of metastatic cells, still remains elusive. Here we used CD133 to mark a specific population from human ovarian cancer cell line and ovarian cancer tissue and determined its hyperactivity in migration and invasion. Therefore, we labeled this population as cancer stem‐like cells (CSLCs). In comparison to CD133− non‐CSLCs, chemokine CCL5 and its receptors, CCR1, CCR3, and CCR5, were consistently upregulated in CSLCs, and most importantly, blocking of CCL5, CCR1, or CCR3 effectively inhibits the invasive capacity of CSLCs. Mechanistically, we identified that this enhanced invasiveness is mediated through nuclear factor κB (NF‐κB) activation and the consequently elevated MMP9 secretion. Our results suggested that the autocrine activation of CCR1 and CCR3 by CCL5 represents one of major mechanisms underlying the metastatic property of ovarian CSLCs. STEM CELLS2012;30:2309–2319 |
| doi_str_mv | 10.1002/stem.1194 |
| format | Article |
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However, how CSCs maintain their invasion and migration abilities, the most important properties of metastatic cells, still remains elusive. Here we used CD133 to mark a specific population from human ovarian cancer cell line and ovarian cancer tissue and determined its hyperactivity in migration and invasion. Therefore, we labeled this population as cancer stem‐like cells (CSLCs). In comparison to CD133− non‐CSLCs, chemokine CCL5 and its receptors, CCR1, CCR3, and CCR5, were consistently upregulated in CSLCs, and most importantly, blocking of CCL5, CCR1, or CCR3 effectively inhibits the invasive capacity of CSLCs. Mechanistically, we identified that this enhanced invasiveness is mediated through nuclear factor κB (NF‐κB) activation and the consequently elevated MMP9 secretion. Our results suggested that the autocrine activation of CCR1 and CCR3 by CCL5 represents one of major mechanisms underlying the metastatic property of ovarian CSLCs. STEM CELLS2012;30:2309–2319</description><identifier>ISSN: 1066-5099</identifier><identifier>EISSN: 1549-4918</identifier><identifier>DOI: 10.1002/stem.1194</identifier><identifier>PMID: 22887854</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>AC133 Antigen ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Biomarkers, Tumor ; Cancer stem cells ; CCL5 ; Cell Line, Tumor ; Cell Movement ; Chemokine CCL5 - antagonists & inhibitors ; Chemokine CCL5 - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Glycoproteins - genetics ; Glycoproteins - metabolism ; Humans ; Invasion ; Matrix Metalloproteinase 9 - genetics ; Matrix Metalloproteinase 9 - secretion ; Migration ; Neoplasm Invasiveness - genetics ; Neoplastic Stem Cells - physiology ; NF-kappa B - genetics ; NF-kappa B - metabolism ; Ovarian ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Ovary - metabolism ; Ovary - pathology ; Peptides - genetics ; Peptides - metabolism ; Primary Cell Culture ; Receptors, CCR1 - antagonists & inhibitors ; Receptors, CCR1 - genetics ; Receptors, CCR3 - antagonists & inhibitors ; Receptors, CCR3 - genetics ; Receptors, CCR5 - genetics ; Receptors, CCR5 - metabolism ; Signal Transduction</subject><ispartof>Stem cells (Dayton, Ohio), 2012-10, Vol.30 (10), p.2309-2319</ispartof><rights>Copyright © 2012 AlphaMed Press</rights><rights>Copyright © 2012 AlphaMed Press.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3134-f9665a826ef19a7ca7cf28703b853c78f1e9d8f453546bf0f49f01c12acb18003</citedby><cites>FETCH-LOGICAL-c3134-f9665a826ef19a7ca7cf28703b853c78f1e9d8f453546bf0f49f01c12acb18003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22887854$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Long, Haixia</creatorcontrib><creatorcontrib>Xie, Rongkai</creatorcontrib><creatorcontrib>Xiang, Tong</creatorcontrib><creatorcontrib>Zhao, Zhongquan</creatorcontrib><creatorcontrib>Lin, Sheng</creatorcontrib><creatorcontrib>Liang, Zhiqing</creatorcontrib><creatorcontrib>Chen, Zhengtang</creatorcontrib><creatorcontrib>Zhu, Bo</creatorcontrib><title>Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133+ Ovarian Cancer Stem-Like Cells via NF-κB-Mediated MMP-9 Upregulation</title><title>Stem cells (Dayton, Ohio)</title><addtitle>STEM CELLS</addtitle><description>The concept of cancer stem cells (CSCs) proposes that solely CSCs are capable of generating tumor metastases. However, how CSCs maintain their invasion and migration abilities, the most important properties of metastatic cells, still remains elusive. Here we used CD133 to mark a specific population from human ovarian cancer cell line and ovarian cancer tissue and determined its hyperactivity in migration and invasion. Therefore, we labeled this population as cancer stem‐like cells (CSLCs). In comparison to CD133− non‐CSLCs, chemokine CCL5 and its receptors, CCR1, CCR3, and CCR5, were consistently upregulated in CSLCs, and most importantly, blocking of CCL5, CCR1, or CCR3 effectively inhibits the invasive capacity of CSLCs. Mechanistically, we identified that this enhanced invasiveness is mediated through nuclear factor κB (NF‐κB) activation and the consequently elevated MMP9 secretion. Our results suggested that the autocrine activation of CCR1 and CCR3 by CCL5 represents one of major mechanisms underlying the metastatic property of ovarian CSLCs. STEM CELLS2012;30:2309–2319</description><subject>AC133 Antigen</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Biomarkers, Tumor</subject><subject>Cancer stem cells</subject><subject>CCL5</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Chemokine CCL5 - antagonists & inhibitors</subject><subject>Chemokine CCL5 - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glycoproteins - genetics</subject><subject>Glycoproteins - metabolism</subject><subject>Humans</subject><subject>Invasion</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Matrix Metalloproteinase 9 - secretion</subject><subject>Migration</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplastic Stem Cells - physiology</subject><subject>NF-kappa B - genetics</subject><subject>NF-kappa B - metabolism</subject><subject>Ovarian</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Ovary - metabolism</subject><subject>Ovary - pathology</subject><subject>Peptides - genetics</subject><subject>Peptides - metabolism</subject><subject>Primary Cell Culture</subject><subject>Receptors, CCR1 - antagonists & inhibitors</subject><subject>Receptors, CCR1 - genetics</subject><subject>Receptors, CCR3 - antagonists & inhibitors</subject><subject>Receptors, CCR3 - genetics</subject><subject>Receptors, CCR5 - genetics</subject><subject>Receptors, CCR5 - metabolism</subject><subject>Signal Transduction</subject><issn>1066-5099</issn><issn>1549-4918</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kNFu0zAUhi0EYmNwwQsgX4KQNzu2E_tyhLVMSrehbuLScl27MkucYieFvQHPxEPwTDi07A7J0vHR-c6nox-A1wSfEoyLszTY7pQQyZ6AY8KZREwS8TT_cVkijqU8Ai9S-ooxYVyI5-CoKISoBGfH4Of5OPQm-mBhXTccLv0m6NaHDbyJfdcPNsHLsNPJ9wHqsIYLv4l6mLrewfojofQ9vN7p6HWAtQ7GRrjM16DG32ejbdsEd17Dqxn6_esDWti114PNmsUNkvBuG-1mbP_6XoJnTrfJvjrUE3A3u7itP6Hmen5ZnzfIUEIZcrIsuRZFaR2RujL5uUJUmK4Ep6YSjli5Fo5xylm5ctgx6TAxpNBmRQTG9AS83Xu3sf822jSozieTD9XB9mNSOTNZYFHRCX23R03sU4rWqW30nY4PGVJT8GoKXk3BZ_bNQTuuOrt-JP8lnYGzPfDdt_bh_ya1vL1YHJRov-Hz8Mfjho73qqxoxdWXq7mqeFPM5uyzaugf6Bqbng</recordid><startdate>201210</startdate><enddate>201210</enddate><creator>Long, Haixia</creator><creator>Xie, Rongkai</creator><creator>Xiang, Tong</creator><creator>Zhao, Zhongquan</creator><creator>Lin, Sheng</creator><creator>Liang, Zhiqing</creator><creator>Chen, Zhengtang</creator><creator>Zhu, Bo</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><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></search><sort><creationdate>201210</creationdate><title>Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133+ Ovarian Cancer Stem-Like Cells via NF-κB-Mediated MMP-9 Upregulation</title><author>Long, Haixia ; Xie, Rongkai ; Xiang, Tong ; Zhao, Zhongquan ; Lin, Sheng ; Liang, Zhiqing ; Chen, Zhengtang ; Zhu, Bo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3134-f9665a826ef19a7ca7cf28703b853c78f1e9d8f453546bf0f49f01c12acb18003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>AC133 Antigen</topic><topic>Antigens, CD - genetics</topic><topic>Antigens, CD - metabolism</topic><topic>Biomarkers, Tumor</topic><topic>Cancer stem cells</topic><topic>CCL5</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Chemokine CCL5 - antagonists & inhibitors</topic><topic>Chemokine CCL5 - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glycoproteins - genetics</topic><topic>Glycoproteins - metabolism</topic><topic>Humans</topic><topic>Invasion</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Matrix Metalloproteinase 9 - secretion</topic><topic>Migration</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neoplastic Stem Cells - physiology</topic><topic>NF-kappa B - genetics</topic><topic>NF-kappa B - metabolism</topic><topic>Ovarian</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Ovary - metabolism</topic><topic>Ovary - pathology</topic><topic>Peptides - genetics</topic><topic>Peptides - metabolism</topic><topic>Primary Cell Culture</topic><topic>Receptors, CCR1 - antagonists & inhibitors</topic><topic>Receptors, CCR1 - genetics</topic><topic>Receptors, CCR3 - antagonists & inhibitors</topic><topic>Receptors, CCR3 - genetics</topic><topic>Receptors, CCR5 - genetics</topic><topic>Receptors, CCR5 - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Long, Haixia</creatorcontrib><creatorcontrib>Xie, Rongkai</creatorcontrib><creatorcontrib>Xiang, Tong</creatorcontrib><creatorcontrib>Zhao, Zhongquan</creatorcontrib><creatorcontrib>Lin, Sheng</creatorcontrib><creatorcontrib>Liang, Zhiqing</creatorcontrib><creatorcontrib>Chen, Zhengtang</creatorcontrib><creatorcontrib>Zhu, Bo</creatorcontrib><collection>Istex</collection><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>Stem cells (Dayton, Ohio)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Long, Haixia</au><au>Xie, Rongkai</au><au>Xiang, Tong</au><au>Zhao, Zhongquan</au><au>Lin, Sheng</au><au>Liang, Zhiqing</au><au>Chen, Zhengtang</au><au>Zhu, Bo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133+ Ovarian Cancer Stem-Like Cells via NF-κB-Mediated MMP-9 Upregulation</atitle><jtitle>Stem cells (Dayton, Ohio)</jtitle><addtitle>STEM CELLS</addtitle><date>2012-10</date><risdate>2012</risdate><volume>30</volume><issue>10</issue><spage>2309</spage><epage>2319</epage><pages>2309-2319</pages><issn>1066-5099</issn><eissn>1549-4918</eissn><abstract>The concept of cancer stem cells (CSCs) proposes that solely CSCs are capable of generating tumor metastases. However, how CSCs maintain their invasion and migration abilities, the most important properties of metastatic cells, still remains elusive. Here we used CD133 to mark a specific population from human ovarian cancer cell line and ovarian cancer tissue and determined its hyperactivity in migration and invasion. Therefore, we labeled this population as cancer stem‐like cells (CSLCs). In comparison to CD133− non‐CSLCs, chemokine CCL5 and its receptors, CCR1, CCR3, and CCR5, were consistently upregulated in CSLCs, and most importantly, blocking of CCL5, CCR1, or CCR3 effectively inhibits the invasive capacity of CSLCs. Mechanistically, we identified that this enhanced invasiveness is mediated through nuclear factor κB (NF‐κB) activation and the consequently elevated MMP9 secretion. Our results suggested that the autocrine activation of CCR1 and CCR3 by CCL5 represents one of major mechanisms underlying the metastatic property of ovarian CSLCs. STEM CELLS2012;30:2309–2319</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22887854</pmid><doi>10.1002/stem.1194</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Stem cells (Dayton, Ohio), 2012-10, Vol.30 (10), p.2309-2319 |
| issn | 1066-5099 1549-4918 |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | AC133 Antigen Antigens, CD - genetics Antigens, CD - metabolism Biomarkers, Tumor Cancer stem cells CCL5 Cell Line, Tumor Cell Movement Chemokine CCL5 - antagonists & inhibitors Chemokine CCL5 - genetics Female Gene Expression Regulation, Neoplastic Glycoproteins - genetics Glycoproteins - metabolism Humans Invasion Matrix Metalloproteinase 9 - genetics Matrix Metalloproteinase 9 - secretion Migration Neoplasm Invasiveness - genetics Neoplastic Stem Cells - physiology NF-kappa B - genetics NF-kappa B - metabolism Ovarian Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Ovary - metabolism Ovary - pathology Peptides - genetics Peptides - metabolism Primary Cell Culture Receptors, CCR1 - antagonists & inhibitors Receptors, CCR1 - genetics Receptors, CCR3 - antagonists & inhibitors Receptors, CCR3 - genetics Receptors, CCR5 - genetics Receptors, CCR5 - metabolism Signal Transduction |
| title | Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133+ Ovarian Cancer Stem-Like Cells via NF-κB-Mediated MMP-9 Upregulation |
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