FOXP3 inhibits cancer stem cell self-renewal via transcriptional repression of COX2 in colorectal cancer cells
Colon cancer stem cell (cCSC) is considered as the seed cell of colon cancer initiation and metastasis. Cyclooxygenase-2 (COX2), a downstream target of NFκB, is found to be essential in promoting cancer stem cell renewal. However, how COX2 is dysregulated in cCSCs is largely unknown. In this study,...
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| Veröffentlicht in: | Oncotarget 2017-07, Vol.8 (27), p.44694-44704 |
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| creator | Liu, Shuo Zhang, Cun Zhang, Kuo Gao, Yuan Wang, Zhaowei Li, Xiaoju Cheng, Guang Wang, Shuning Xue, Xiaochang Li, Weina Zhang, Wei Zhang, Yingqi Xing, Xianghui Li, Meng Hao, Qiang |
| description | Colon cancer stem cell (cCSC) is considered as the seed cell of colon cancer initiation and metastasis. Cyclooxygenase-2 (COX2), a downstream target of NFκB, is found to be essential in promoting cancer stem cell renewal. However, how COX2 is dysregulated in cCSCs is largely unknown. In this study, we found that the expression of transcription factor FOXP3 was much lower in the spheroids than that in the parental tumor cells. Overexpression of FOXP3 significantly decreased the numbers of spheres, reduced the side population. Accordingly, FOXP3 expression decreased the tumor size and weight in the xenograft model. The tumor inhibitory effects of FOXP3 were rarely seen when COX2 was additionally knocked down. Mechanically, FOXP3 transcriptionally repressed COX2 expression via interacting with and thus inhibiting p65 activity on the putative NFκB response elements in COX2 promoter. Taken together, we here revealed possible involvement of FOXP3 in regulating cCSC self-renewal via tuning COX2 expression, and thus providing a new target for the eradication of colon cancer stem cells. |
| doi_str_mv | 10.18632/oncotarget.17974 |
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Cyclooxygenase-2 (COX2), a downstream target of NFκB, is found to be essential in promoting cancer stem cell renewal. However, how COX2 is dysregulated in cCSCs is largely unknown. In this study, we found that the expression of transcription factor FOXP3 was much lower in the spheroids than that in the parental tumor cells. Overexpression of FOXP3 significantly decreased the numbers of spheres, reduced the side population. Accordingly, FOXP3 expression decreased the tumor size and weight in the xenograft model. The tumor inhibitory effects of FOXP3 were rarely seen when COX2 was additionally knocked down. Mechanically, FOXP3 transcriptionally repressed COX2 expression via interacting with and thus inhibiting p65 activity on the putative NFκB response elements in COX2 promoter. Taken together, we here revealed possible involvement of FOXP3 in regulating cCSC self-renewal via tuning COX2 expression, and thus providing a new target for the eradication of colon cancer stem cells.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.17974</identifier><identifier>PMID: 28591725</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Animals ; Cell Line, Tumor ; Cell Self Renewal - genetics ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Cyclooxygenase 2 - genetics ; Cyclooxygenase 2 - metabolism ; Disease Models, Animal ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; Gene Expression Regulation ; Gene Expression Regulation, Neoplastic ; Heterografts ; Humans ; Mice ; Neoplastic Stem Cells - metabolism ; NF-kappa B - metabolism ; Promoter Regions, Genetic ; Protein Binding ; Research Paper ; Transcription, Genetic</subject><ispartof>Oncotarget, 2017-07, Vol.8 (27), p.44694-44704</ispartof><rights>Copyright: © 2017 Liu et al. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-59a12564bd6961479c0dfe7412225d18c0c33c468859ba31c3076f335e7ddcdc3</citedby><cites>FETCH-LOGICAL-c356t-59a12564bd6961479c0dfe7412225d18c0c33c468859ba31c3076f335e7ddcdc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5546511/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5546511/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28591725$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Shuo</creatorcontrib><creatorcontrib>Zhang, Cun</creatorcontrib><creatorcontrib>Zhang, Kuo</creatorcontrib><creatorcontrib>Gao, Yuan</creatorcontrib><creatorcontrib>Wang, Zhaowei</creatorcontrib><creatorcontrib>Li, Xiaoju</creatorcontrib><creatorcontrib>Cheng, Guang</creatorcontrib><creatorcontrib>Wang, Shuning</creatorcontrib><creatorcontrib>Xue, Xiaochang</creatorcontrib><creatorcontrib>Li, Weina</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><creatorcontrib>Zhang, Yingqi</creatorcontrib><creatorcontrib>Xing, Xianghui</creatorcontrib><creatorcontrib>Li, Meng</creatorcontrib><creatorcontrib>Hao, Qiang</creatorcontrib><title>FOXP3 inhibits cancer stem cell self-renewal via transcriptional repression of COX2 in colorectal cancer cells</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Colon cancer stem cell (cCSC) is considered as the seed cell of colon cancer initiation and metastasis. Cyclooxygenase-2 (COX2), a downstream target of NFκB, is found to be essential in promoting cancer stem cell renewal. However, how COX2 is dysregulated in cCSCs is largely unknown. In this study, we found that the expression of transcription factor FOXP3 was much lower in the spheroids than that in the parental tumor cells. Overexpression of FOXP3 significantly decreased the numbers of spheres, reduced the side population. Accordingly, FOXP3 expression decreased the tumor size and weight in the xenograft model. The tumor inhibitory effects of FOXP3 were rarely seen when COX2 was additionally knocked down. Mechanically, FOXP3 transcriptionally repressed COX2 expression via interacting with and thus inhibiting p65 activity on the putative NFκB response elements in COX2 promoter. Taken together, we here revealed possible involvement of FOXP3 in regulating cCSC self-renewal via tuning COX2 expression, and thus providing a new target for the eradication of colon cancer stem cells.</description><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Cell Self Renewal - genetics</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Cyclooxygenase 2 - genetics</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Disease Models, Animal</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Heterografts</subject><subject>Humans</subject><subject>Mice</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Binding</subject><subject>Research Paper</subject><subject>Transcription, Genetic</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU1PHDEMhiNUVBDwA3pBOfYydPI9uVSqVqUgIS0HkLhFWY8HUs0m2yRL1X_fAFuguTiOXz-x9RLyifVnbNCCf0kRUvX5HusZM9bIPXLIrLQdV0p8eHc_ICel_OzbUdIM3H4kB3xQlhmuDkk8X95dCxriQ1iFWij4CJhpqbimgPNMC85TlzHibz_Tx-BpzT4WyGFTQ4rtLeMmYyktoWmii-UdbzQKaU4ZoTbBDvlEK8dkf_JzwZNdPCK3599vFhfd1fLH5eLbVQdC6dop6xlXWq5GbTWTxkI_Tmgk45yrkQ3QgxAg9dD2WHnBQPRGT0IoNOMII4gj8vWFu9mu1jgCxjb27DY5rH3-45IP7v9KDA_uPj06paRWjDXA5x0gp19bLNWtQ3lawUdM2-KY7Y3g0va6SdmLFHIqJeP0-g3r3bNV7s0q92xV6zl9P99rxz9jxF-2SZQA</recordid><startdate>20170704</startdate><enddate>20170704</enddate><creator>Liu, Shuo</creator><creator>Zhang, Cun</creator><creator>Zhang, Kuo</creator><creator>Gao, Yuan</creator><creator>Wang, Zhaowei</creator><creator>Li, Xiaoju</creator><creator>Cheng, Guang</creator><creator>Wang, Shuning</creator><creator>Xue, Xiaochang</creator><creator>Li, Weina</creator><creator>Zhang, Wei</creator><creator>Zhang, Yingqi</creator><creator>Xing, Xianghui</creator><creator>Li, Meng</creator><creator>Hao, Qiang</creator><general>Impact Journals LLC</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><scope>5PM</scope></search><sort><creationdate>20170704</creationdate><title>FOXP3 inhibits cancer stem cell self-renewal via transcriptional repression of COX2 in colorectal cancer cells</title><author>Liu, Shuo ; Zhang, Cun ; Zhang, Kuo ; Gao, Yuan ; Wang, Zhaowei ; Li, Xiaoju ; Cheng, Guang ; Wang, Shuning ; Xue, Xiaochang ; Li, Weina ; Zhang, Wei ; Zhang, Yingqi ; Xing, Xianghui ; Li, Meng ; Hao, Qiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-59a12564bd6961479c0dfe7412225d18c0c33c468859ba31c3076f335e7ddcdc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Cell Self Renewal - genetics</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Cyclooxygenase 2 - genetics</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Disease Models, Animal</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Heterografts</topic><topic>Humans</topic><topic>Mice</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Binding</topic><topic>Research Paper</topic><topic>Transcription, Genetic</topic><toplevel>online_resources</toplevel><creatorcontrib>Liu, Shuo</creatorcontrib><creatorcontrib>Zhang, Cun</creatorcontrib><creatorcontrib>Zhang, Kuo</creatorcontrib><creatorcontrib>Gao, Yuan</creatorcontrib><creatorcontrib>Wang, Zhaowei</creatorcontrib><creatorcontrib>Li, Xiaoju</creatorcontrib><creatorcontrib>Cheng, Guang</creatorcontrib><creatorcontrib>Wang, Shuning</creatorcontrib><creatorcontrib>Xue, Xiaochang</creatorcontrib><creatorcontrib>Li, Weina</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><creatorcontrib>Zhang, Yingqi</creatorcontrib><creatorcontrib>Xing, Xianghui</creatorcontrib><creatorcontrib>Li, Meng</creatorcontrib><creatorcontrib>Hao, Qiang</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>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Shuo</au><au>Zhang, Cun</au><au>Zhang, Kuo</au><au>Gao, Yuan</au><au>Wang, Zhaowei</au><au>Li, Xiaoju</au><au>Cheng, Guang</au><au>Wang, Shuning</au><au>Xue, Xiaochang</au><au>Li, Weina</au><au>Zhang, Wei</au><au>Zhang, Yingqi</au><au>Xing, Xianghui</au><au>Li, Meng</au><au>Hao, Qiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FOXP3 inhibits cancer stem cell self-renewal via transcriptional repression of COX2 in colorectal cancer cells</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2017-07-04</date><risdate>2017</risdate><volume>8</volume><issue>27</issue><spage>44694</spage><epage>44704</epage><pages>44694-44704</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>Colon cancer stem cell (cCSC) is considered as the seed cell of colon cancer initiation and metastasis. Cyclooxygenase-2 (COX2), a downstream target of NFκB, is found to be essential in promoting cancer stem cell renewal. However, how COX2 is dysregulated in cCSCs is largely unknown. In this study, we found that the expression of transcription factor FOXP3 was much lower in the spheroids than that in the parental tumor cells. Overexpression of FOXP3 significantly decreased the numbers of spheres, reduced the side population. Accordingly, FOXP3 expression decreased the tumor size and weight in the xenograft model. The tumor inhibitory effects of FOXP3 were rarely seen when COX2 was additionally knocked down. Mechanically, FOXP3 transcriptionally repressed COX2 expression via interacting with and thus inhibiting p65 activity on the putative NFκB response elements in COX2 promoter. 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| subjects | Animals Cell Line, Tumor Cell Self Renewal - genetics Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Cyclooxygenase 2 - genetics Cyclooxygenase 2 - metabolism Disease Models, Animal Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Regulation Gene Expression Regulation, Neoplastic Heterografts Humans Mice Neoplastic Stem Cells - metabolism NF-kappa B - metabolism Promoter Regions, Genetic Protein Binding Research Paper Transcription, Genetic |
| title | FOXP3 inhibits cancer stem cell self-renewal via transcriptional repression of COX2 in colorectal cancer cells |
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