PTX3 gene activation in EGF-induced head and neck cancer cell metastasis
Overexpression of the epidermal growth factor (EGF) receptor (EGFR) is associated with enhanced invasion and metastasis in head and neck squamous cell carcinoma (HNSCC). Long Pentraxin PTX3 is involved in immune escape in cancer cells. Here, we identified PTX3 as a promoting factor that mediates EGF...
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| creator | Chang, Wei-Chiao Wu, Shuo-Lun Huang, Wan-Chen Hsu, Jinn-Yuan Chan, Shih-Hung Wang, Ju-Ming Tsai, Jhih-Peng Chen, Ben-Kuen |
| description | Overexpression of the epidermal growth factor (EGF) receptor (EGFR) is associated with enhanced invasion and metastasis in head and neck squamous cell carcinoma (HNSCC). Long Pentraxin PTX3 is involved in immune escape in cancer cells. Here, we identified PTX3 as a promoting factor that mediates EGF-induced HNSCC metastasis. EGF-induced PTX3 transcriptional activation is via the binding of c-Jun to the activator protein (AP)-1 binding site of the PTX3 promoter. PI3K/Akt and NF-κB were essential for the PTX3 activation. EGF-induced PTX3 expression was blocked in c-Jun- and NF-κB-knockdown cells. EGF-mediated PTX3 secretion resulted in the enhancement of cell migration and invasion, and interactions between cancer and endothelial cells. The tail-vein injection animal model revealed that depletion of PTX3 decreased EGF-primed tumor cell metastatic seeding of the lungs. In addition, fibronectin, matrix metalloproteinase-9 (MMP9) and E-cadherin were essential components in EGFR/PTX3-mediated cancer metastasis. In conclusion, PI3K/Akt and NF-κB-dependent regulation of AP-1 mediates PTX3 transcriptional responses to EGF. Autocrine production of EGF-induced PTX3 in turn induces metastatic molecules, activating inflammatory cascades and metastasis. |
| doi_str_mv | 10.18632/oncotarget.3482 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4480713</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1677890122</sourcerecordid><originalsourceid>FETCH-LOGICAL-c396t-ff7682f689615f9c64336e756fcc39d4cc7af73583c4b9e976f9217b62f33a473</originalsourceid><addsrcrecordid>eNpVUUtLAzEQDqJoqd49SY5eVjePzeMiSGmtIOihgreQZic1uputm13Bf-9qtdZhYAbmm28eH0KnJL8gSjB62UTXdLZdQXfBuKJ7aEQ01xktCra_kx-hk5Re8sEKLhXVh-iIFlJLWqgRmj8snhheQQRsXRfebReaiEPE05tZFmLZOyjxM9gS21jiCO4VOxsdtNhBVeEaOpsGD-kYHXhbJTj5iWP0OJsuJvPs7v7mdnJ9lzmmRZd5L4WiXigtSOG1E5wxAbIQ3g2AkjsnrZesUMzxpQYthdeUyKWgnjHLJRujqw3vul_WUDqIXWsrs25DbdsP09hg_ldieDar5t1wrnJJ2EBw_kPQNm89pM7UIX0dYyM0fTJESKl0TigdoPkG6tompRb8dgzJzbcG5k8D86XB0HK2u9624ffj7BMohYTm</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1677890122</pqid></control><display><type>article</type><title>PTX3 gene activation in EGF-induced head and neck cancer cell metastasis</title><source>MEDLINE</source><source>PubMed Central Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free E- Journals</source><creator>Chang, Wei-Chiao ; Wu, Shuo-Lun ; Huang, Wan-Chen ; Hsu, Jinn-Yuan ; Chan, Shih-Hung ; Wang, Ju-Ming ; Tsai, Jhih-Peng ; Chen, Ben-Kuen</creator><creatorcontrib>Chang, Wei-Chiao ; Wu, Shuo-Lun ; Huang, Wan-Chen ; Hsu, Jinn-Yuan ; Chan, Shih-Hung ; Wang, Ju-Ming ; Tsai, Jhih-Peng ; Chen, Ben-Kuen</creatorcontrib><description>Overexpression of the epidermal growth factor (EGF) receptor (EGFR) is associated with enhanced invasion and metastasis in head and neck squamous cell carcinoma (HNSCC). Long Pentraxin PTX3 is involved in immune escape in cancer cells. Here, we identified PTX3 as a promoting factor that mediates EGF-induced HNSCC metastasis. EGF-induced PTX3 transcriptional activation is via the binding of c-Jun to the activator protein (AP)-1 binding site of the PTX3 promoter. PI3K/Akt and NF-κB were essential for the PTX3 activation. EGF-induced PTX3 expression was blocked in c-Jun- and NF-κB-knockdown cells. EGF-mediated PTX3 secretion resulted in the enhancement of cell migration and invasion, and interactions between cancer and endothelial cells. The tail-vein injection animal model revealed that depletion of PTX3 decreased EGF-primed tumor cell metastatic seeding of the lungs. In addition, fibronectin, matrix metalloproteinase-9 (MMP9) and E-cadherin were essential components in EGFR/PTX3-mediated cancer metastasis. In conclusion, PI3K/Akt and NF-κB-dependent regulation of AP-1 mediates PTX3 transcriptional responses to EGF. Autocrine production of EGF-induced PTX3 in turn induces metastatic molecules, activating inflammatory cascades and metastasis.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.3482</identifier><identifier>PMID: 25797258</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Animals ; C-Reactive Protein - biosynthesis ; C-Reactive Protein - genetics ; C-Reactive Protein - metabolism ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell Line, Tumor ; Cell Movement - genetics ; Epidermal Growth Factor - metabolism ; Epidermal Growth Factor - pharmacology ; ErbB Receptors - genetics ; ErbB Receptors - metabolism ; Gene Expression Regulation, Neoplastic ; Head and Neck Neoplasms - genetics ; Head and Neck Neoplasms - pathology ; Heterografts ; Humans ; JNK Mitogen-Activated Protein Kinases - metabolism ; Male ; Mice ; Mice, SCID ; Neoplasm Metastasis ; NF-kappa B - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-akt - metabolism ; Research Paper ; Serum Amyloid P-Component - biosynthesis ; Serum Amyloid P-Component - genetics ; Serum Amyloid P-Component - metabolism ; Signal Transduction ; Squamous Cell Carcinoma of Head and Neck ; Transcription Factor AP-1 - metabolism ; Transfection</subject><ispartof>Oncotarget, 2015-04, Vol.6 (10), p.7741-7757</ispartof><rights>Copyright: © 2015 Chang et al. 2015</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-ff7682f689615f9c64336e756fcc39d4cc7af73583c4b9e976f9217b62f33a473</citedby><cites>FETCH-LOGICAL-c396t-ff7682f689615f9c64336e756fcc39d4cc7af73583c4b9e976f9217b62f33a473</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/PMC4480713/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480713/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25797258$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, Wei-Chiao</creatorcontrib><creatorcontrib>Wu, Shuo-Lun</creatorcontrib><creatorcontrib>Huang, Wan-Chen</creatorcontrib><creatorcontrib>Hsu, Jinn-Yuan</creatorcontrib><creatorcontrib>Chan, Shih-Hung</creatorcontrib><creatorcontrib>Wang, Ju-Ming</creatorcontrib><creatorcontrib>Tsai, Jhih-Peng</creatorcontrib><creatorcontrib>Chen, Ben-Kuen</creatorcontrib><title>PTX3 gene activation in EGF-induced head and neck cancer cell metastasis</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Overexpression of the epidermal growth factor (EGF) receptor (EGFR) is associated with enhanced invasion and metastasis in head and neck squamous cell carcinoma (HNSCC). Long Pentraxin PTX3 is involved in immune escape in cancer cells. Here, we identified PTX3 as a promoting factor that mediates EGF-induced HNSCC metastasis. EGF-induced PTX3 transcriptional activation is via the binding of c-Jun to the activator protein (AP)-1 binding site of the PTX3 promoter. PI3K/Akt and NF-κB were essential for the PTX3 activation. EGF-induced PTX3 expression was blocked in c-Jun- and NF-κB-knockdown cells. EGF-mediated PTX3 secretion resulted in the enhancement of cell migration and invasion, and interactions between cancer and endothelial cells. The tail-vein injection animal model revealed that depletion of PTX3 decreased EGF-primed tumor cell metastatic seeding of the lungs. In addition, fibronectin, matrix metalloproteinase-9 (MMP9) and E-cadherin were essential components in EGFR/PTX3-mediated cancer metastasis. In conclusion, PI3K/Akt and NF-κB-dependent regulation of AP-1 mediates PTX3 transcriptional responses to EGF. Autocrine production of EGF-induced PTX3 in turn induces metastatic molecules, activating inflammatory cascades and metastasis.</description><subject>Animals</subject><subject>C-Reactive Protein - biosynthesis</subject><subject>C-Reactive Protein - genetics</subject><subject>C-Reactive Protein - metabolism</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>Epidermal Growth Factor - pharmacology</subject><subject>ErbB Receptors - genetics</subject><subject>ErbB Receptors - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Head and Neck Neoplasms - genetics</subject><subject>Head and Neck Neoplasms - pathology</subject><subject>Heterografts</subject><subject>Humans</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Neoplasm Metastasis</subject><subject>NF-kappa B - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Research Paper</subject><subject>Serum Amyloid P-Component - biosynthesis</subject><subject>Serum Amyloid P-Component - genetics</subject><subject>Serum Amyloid P-Component - metabolism</subject><subject>Signal Transduction</subject><subject>Squamous Cell Carcinoma of Head and Neck</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transfection</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUUtLAzEQDqJoqd49SY5eVjePzeMiSGmtIOihgreQZic1uputm13Bf-9qtdZhYAbmm28eH0KnJL8gSjB62UTXdLZdQXfBuKJ7aEQ01xktCra_kx-hk5Re8sEKLhXVh-iIFlJLWqgRmj8snhheQQRsXRfebReaiEPE05tZFmLZOyjxM9gS21jiCO4VOxsdtNhBVeEaOpsGD-kYHXhbJTj5iWP0OJsuJvPs7v7mdnJ9lzmmRZd5L4WiXigtSOG1E5wxAbIQ3g2AkjsnrZesUMzxpQYthdeUyKWgnjHLJRujqw3vul_WUDqIXWsrs25DbdsP09hg_ldieDar5t1wrnJJ2EBw_kPQNm89pM7UIX0dYyM0fTJESKl0TigdoPkG6tompRb8dgzJzbcG5k8D86XB0HK2u9624ffj7BMohYTm</recordid><startdate>20150410</startdate><enddate>20150410</enddate><creator>Chang, Wei-Chiao</creator><creator>Wu, Shuo-Lun</creator><creator>Huang, Wan-Chen</creator><creator>Hsu, Jinn-Yuan</creator><creator>Chan, Shih-Hung</creator><creator>Wang, Ju-Ming</creator><creator>Tsai, Jhih-Peng</creator><creator>Chen, Ben-Kuen</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>20150410</creationdate><title>PTX3 gene activation in EGF-induced head and neck cancer cell metastasis</title><author>Chang, Wei-Chiao ; Wu, Shuo-Lun ; Huang, Wan-Chen ; Hsu, Jinn-Yuan ; Chan, Shih-Hung ; Wang, Ju-Ming ; Tsai, Jhih-Peng ; Chen, Ben-Kuen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-ff7682f689615f9c64336e756fcc39d4cc7af73583c4b9e976f9217b62f33a473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>C-Reactive Protein - biosynthesis</topic><topic>C-Reactive Protein - genetics</topic><topic>C-Reactive Protein - metabolism</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>Epidermal Growth Factor - pharmacology</topic><topic>ErbB Receptors - genetics</topic><topic>ErbB Receptors - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Head and Neck Neoplasms - genetics</topic><topic>Head and Neck Neoplasms - pathology</topic><topic>Heterografts</topic><topic>Humans</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>Neoplasm Metastasis</topic><topic>NF-kappa B - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Research Paper</topic><topic>Serum Amyloid P-Component - biosynthesis</topic><topic>Serum Amyloid P-Component - genetics</topic><topic>Serum Amyloid P-Component - metabolism</topic><topic>Signal Transduction</topic><topic>Squamous Cell Carcinoma of Head and Neck</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Transfection</topic><toplevel>online_resources</toplevel><creatorcontrib>Chang, Wei-Chiao</creatorcontrib><creatorcontrib>Wu, Shuo-Lun</creatorcontrib><creatorcontrib>Huang, Wan-Chen</creatorcontrib><creatorcontrib>Hsu, Jinn-Yuan</creatorcontrib><creatorcontrib>Chan, Shih-Hung</creatorcontrib><creatorcontrib>Wang, Ju-Ming</creatorcontrib><creatorcontrib>Tsai, Jhih-Peng</creatorcontrib><creatorcontrib>Chen, Ben-Kuen</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>Chang, Wei-Chiao</au><au>Wu, Shuo-Lun</au><au>Huang, Wan-Chen</au><au>Hsu, Jinn-Yuan</au><au>Chan, Shih-Hung</au><au>Wang, Ju-Ming</au><au>Tsai, Jhih-Peng</au><au>Chen, Ben-Kuen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PTX3 gene activation in EGF-induced head and neck cancer cell metastasis</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2015-04-10</date><risdate>2015</risdate><volume>6</volume><issue>10</issue><spage>7741</spage><epage>7757</epage><pages>7741-7757</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>Overexpression of the epidermal growth factor (EGF) receptor (EGFR) is associated with enhanced invasion and metastasis in head and neck squamous cell carcinoma (HNSCC). Long Pentraxin PTX3 is involved in immune escape in cancer cells. Here, we identified PTX3 as a promoting factor that mediates EGF-induced HNSCC metastasis. EGF-induced PTX3 transcriptional activation is via the binding of c-Jun to the activator protein (AP)-1 binding site of the PTX3 promoter. PI3K/Akt and NF-κB were essential for the PTX3 activation. EGF-induced PTX3 expression was blocked in c-Jun- and NF-κB-knockdown cells. EGF-mediated PTX3 secretion resulted in the enhancement of cell migration and invasion, and interactions between cancer and endothelial cells. The tail-vein injection animal model revealed that depletion of PTX3 decreased EGF-primed tumor cell metastatic seeding of the lungs. In addition, fibronectin, matrix metalloproteinase-9 (MMP9) and E-cadherin were essential components in EGFR/PTX3-mediated cancer metastasis. In conclusion, PI3K/Akt and NF-κB-dependent regulation of AP-1 mediates PTX3 transcriptional responses to EGF. Autocrine production of EGF-induced PTX3 in turn induces metastatic molecules, activating inflammatory cascades and metastasis.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>25797258</pmid><doi>10.18632/oncotarget.3482</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals C-Reactive Protein - biosynthesis C-Reactive Protein - genetics C-Reactive Protein - metabolism Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell Line, Tumor Cell Movement - genetics Epidermal Growth Factor - metabolism Epidermal Growth Factor - pharmacology ErbB Receptors - genetics ErbB Receptors - metabolism Gene Expression Regulation, Neoplastic Head and Neck Neoplasms - genetics Head and Neck Neoplasms - pathology Heterografts Humans JNK Mitogen-Activated Protein Kinases - metabolism Male Mice Mice, SCID Neoplasm Metastasis NF-kappa B - metabolism Phosphatidylinositol 3-Kinases - metabolism Promoter Regions, Genetic Proto-Oncogene Proteins c-akt - metabolism Research Paper Serum Amyloid P-Component - biosynthesis Serum Amyloid P-Component - genetics Serum Amyloid P-Component - metabolism Signal Transduction Squamous Cell Carcinoma of Head and Neck Transcription Factor AP-1 - metabolism Transfection |
| title | PTX3 gene activation in EGF-induced head and neck cancer cell metastasis |
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