Celecoxib suppresses proliferation and metastasis of pancreatic cancer cells by down-regulating STAT3 / NF-kB and L1CAM activities
To explore the molecular mechanisms of celecoxib-induced pancreatic cancer suppression in vivo and in vitro. The anti-pancreatic cancer activities of celecoxib (0, 20, 60 and 100 μmol/L) were investigated by cell viability and migration of Panc-1 and Bxpc-3 cells in vitro. The expression of L1CAM in...
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| Veröffentlicht in: | Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] 2018-04, Vol.18 (3), p.328-333 |
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| container_title | Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] |
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| creator | Zuo, Chaohui Hong, Yuan Qiu, Xiaoxin Yang, Darong Liu, Nianli Sheng, Xinyi Zhou, Kunyan Tang, Bo Xiong, Shuhan Ma, Min Liu, Zhuo |
| description | To explore the molecular mechanisms of celecoxib-induced pancreatic cancer suppression in vivo and in vitro.
The anti-pancreatic cancer activities of celecoxib (0, 20, 60 and 100 μmol/L) were investigated by cell viability and migration of Panc-1 and Bxpc-3 cells in vitro. The expression of L1CAM in pancreatic cancer and adjacent tissues was compared using immunohistochemistry. The expressions of L1CAM, STAT3, p-STAT3, NF-κB, p-NF-κB were determined by western blotting, and cell invasive ability was determined by wound healing assay in L1CAM-silenced and over-expressed Panc-1and Bxpc-3 cells.
The expression of L1CAM in pancreatic carcinoma was stronger than that in the adjacent tissues and L1CAM could increase the growth and invasion of pancreatic cancer cells. Over-expression of L1CAM activated the STAT3/NF-κB signaling pathway in Panc-1 and Bxpc-3 pancreatic cancer cells and celecoxib inhibited their viability and the expressions of STAT3, p-STAT3, NF-κB, p-NF-κB as well as full length L1CAM in a concentration dependent manner.
L1CAM was highly expressed in pancreatic cancer tissue and positively correlated with age, TNM staging and tumor differentiation. L1CAM activated the STAT/NF-κB signaling pathway and celecoxib could inhibit the activity of L1CAM, STAT3 and the NF-κB signaling pathway resulting in decreased growth and invasion of pancreatic cancer cells. |
| doi_str_mv | 10.1016/j.pan.2018.02.006 |
| format | Article |
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The anti-pancreatic cancer activities of celecoxib (0, 20, 60 and 100 μmol/L) were investigated by cell viability and migration of Panc-1 and Bxpc-3 cells in vitro. The expression of L1CAM in pancreatic cancer and adjacent tissues was compared using immunohistochemistry. The expressions of L1CAM, STAT3, p-STAT3, NF-κB, p-NF-κB were determined by western blotting, and cell invasive ability was determined by wound healing assay in L1CAM-silenced and over-expressed Panc-1and Bxpc-3 cells.
The expression of L1CAM in pancreatic carcinoma was stronger than that in the adjacent tissues and L1CAM could increase the growth and invasion of pancreatic cancer cells. Over-expression of L1CAM activated the STAT3/NF-κB signaling pathway in Panc-1 and Bxpc-3 pancreatic cancer cells and celecoxib inhibited their viability and the expressions of STAT3, p-STAT3, NF-κB, p-NF-κB as well as full length L1CAM in a concentration dependent manner.
L1CAM was highly expressed in pancreatic cancer tissue and positively correlated with age, TNM staging and tumor differentiation. L1CAM activated the STAT/NF-κB signaling pathway and celecoxib could inhibit the activity of L1CAM, STAT3 and the NF-κB signaling pathway resulting in decreased growth and invasion of pancreatic cancer cells.</description><identifier>ISSN: 1424-3903</identifier><identifier>EISSN: 1424-3911</identifier><identifier>DOI: 10.1016/j.pan.2018.02.006</identifier><identifier>PMID: 29525378</identifier><language>eng</language><publisher>Switzerland: Elsevier B.V</publisher><subject>Angiogenesis ; Cancer therapies ; Celecoxib ; Cell adhesion & migration ; Cell migration ; Cell proliferation ; Chemotherapy ; Immunoglobulins ; Immunohistochemistry ; Invasiveness ; L1CAM ; Medical research ; Membranes ; Metastases ; Metastasis ; Molecular modelling ; Mortality ; NF-κB protein ; Overexpression ; Pancreatic cancer ; Pancreatic carcinoma ; Signal transduction ; Stat3 protein ; STAT3/NF-kB ; Tumors ; Western blotting ; Wound healing</subject><ispartof>Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2018-04, Vol.18 (3), p.328-333</ispartof><rights>2018</rights><rights>Copyright © 2018. Published by Elsevier B.V.</rights><rights>Copyright Elsevier Limited Apr 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-d5b0ad3c152cad95072dbee52c26e1d3715808e566f7dc7314dc576d8cf162e43</citedby><cites>FETCH-LOGICAL-c381t-d5b0ad3c152cad95072dbee52c26e1d3715808e566f7dc7314dc576d8cf162e43</cites><orcidid>0000-0002-0835-7464</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29525378$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zuo, Chaohui</creatorcontrib><creatorcontrib>Hong, Yuan</creatorcontrib><creatorcontrib>Qiu, Xiaoxin</creatorcontrib><creatorcontrib>Yang, Darong</creatorcontrib><creatorcontrib>Liu, Nianli</creatorcontrib><creatorcontrib>Sheng, Xinyi</creatorcontrib><creatorcontrib>Zhou, Kunyan</creatorcontrib><creatorcontrib>Tang, Bo</creatorcontrib><creatorcontrib>Xiong, Shuhan</creatorcontrib><creatorcontrib>Ma, Min</creatorcontrib><creatorcontrib>Liu, Zhuo</creatorcontrib><title>Celecoxib suppresses proliferation and metastasis of pancreatic cancer cells by down-regulating STAT3 / NF-kB and L1CAM activities</title><title>Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]</title><addtitle>Pancreatology</addtitle><description>To explore the molecular mechanisms of celecoxib-induced pancreatic cancer suppression in vivo and in vitro.
The anti-pancreatic cancer activities of celecoxib (0, 20, 60 and 100 μmol/L) were investigated by cell viability and migration of Panc-1 and Bxpc-3 cells in vitro. The expression of L1CAM in pancreatic cancer and adjacent tissues was compared using immunohistochemistry. The expressions of L1CAM, STAT3, p-STAT3, NF-κB, p-NF-κB were determined by western blotting, and cell invasive ability was determined by wound healing assay in L1CAM-silenced and over-expressed Panc-1and Bxpc-3 cells.
The expression of L1CAM in pancreatic carcinoma was stronger than that in the adjacent tissues and L1CAM could increase the growth and invasion of pancreatic cancer cells. Over-expression of L1CAM activated the STAT3/NF-κB signaling pathway in Panc-1 and Bxpc-3 pancreatic cancer cells and celecoxib inhibited their viability and the expressions of STAT3, p-STAT3, NF-κB, p-NF-κB as well as full length L1CAM in a concentration dependent manner.
L1CAM was highly expressed in pancreatic cancer tissue and positively correlated with age, TNM staging and tumor differentiation. L1CAM activated the STAT/NF-κB signaling pathway and celecoxib could inhibit the activity of L1CAM, STAT3 and the NF-κB signaling pathway resulting in decreased growth and invasion of pancreatic cancer cells.</description><subject>Angiogenesis</subject><subject>Cancer therapies</subject><subject>Celecoxib</subject><subject>Cell adhesion & migration</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Chemotherapy</subject><subject>Immunoglobulins</subject><subject>Immunohistochemistry</subject><subject>Invasiveness</subject><subject>L1CAM</subject><subject>Medical research</subject><subject>Membranes</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Molecular modelling</subject><subject>Mortality</subject><subject>NF-κB protein</subject><subject>Overexpression</subject><subject>Pancreatic cancer</subject><subject>Pancreatic carcinoma</subject><subject>Signal transduction</subject><subject>Stat3 protein</subject><subject>STAT3/NF-kB</subject><subject>Tumors</subject><subject>Western blotting</subject><subject>Wound healing</subject><issn>1424-3903</issn><issn>1424-3911</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kU1v1DAQhi0EoqXlB3BBlrhwSeqxN4mjnpYVhUrb9tDt2XLsSeUlG6d20o8rvxyHbXvggGTJY80z74zfIeQTsBwYlCfbfNB9zhnInPGcsfINOYQFX2SiBnj7GjNxQD7EuGWMc4D6PTngdcELUclD8nuFHRr_6Boap2EIGCNGOgTfuRaDHp3vqe4t3eGoYzouUt_S1NYETFlDTQoxUINdF2nzRK1_6LOAt1OX0v0tvd4sN4Ke0Muz7Ne3v1JrWC0vqDaju3ejw3hM3rW6i_jx-T4iN2ffN6uf2frqx_lquc6MkDBmtmiYtsJAwY22dcEqbhvE9OIlghUVFJJJLMqyraypBCysKarSStNCyXEhjsjXvW763d2EcVQ7F-e5dY9-iir5KIAJJmf0yz_o1k-hT9PNVC1TL-CJgj1lgo8xYKuG4HY6PClgal6Q2qrk1FwiFeMqLSjVfH5Wnpod2teKl40k4HQPYLLi3mFQ0ThMHlsX0IzKevcf-T8ZZKBe</recordid><startdate>201804</startdate><enddate>201804</enddate><creator>Zuo, Chaohui</creator><creator>Hong, Yuan</creator><creator>Qiu, Xiaoxin</creator><creator>Yang, Darong</creator><creator>Liu, Nianli</creator><creator>Sheng, Xinyi</creator><creator>Zhou, Kunyan</creator><creator>Tang, Bo</creator><creator>Xiong, Shuhan</creator><creator>Ma, Min</creator><creator>Liu, Zhuo</creator><general>Elsevier B.V</general><general>Elsevier Limited</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0835-7464</orcidid></search><sort><creationdate>201804</creationdate><title>Celecoxib suppresses proliferation and metastasis of pancreatic cancer cells by down-regulating STAT3 / NF-kB and L1CAM activities</title><author>Zuo, Chaohui ; Hong, Yuan ; Qiu, Xiaoxin ; Yang, Darong ; Liu, Nianli ; Sheng, Xinyi ; Zhou, Kunyan ; Tang, Bo ; Xiong, Shuhan ; Ma, Min ; Liu, Zhuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-d5b0ad3c152cad95072dbee52c26e1d3715808e566f7dc7314dc576d8cf162e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Angiogenesis</topic><topic>Cancer therapies</topic><topic>Celecoxib</topic><topic>Cell adhesion & migration</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Chemotherapy</topic><topic>Immunoglobulins</topic><topic>Immunohistochemistry</topic><topic>Invasiveness</topic><topic>L1CAM</topic><topic>Medical research</topic><topic>Membranes</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Molecular modelling</topic><topic>Mortality</topic><topic>NF-κB protein</topic><topic>Overexpression</topic><topic>Pancreatic cancer</topic><topic>Pancreatic carcinoma</topic><topic>Signal transduction</topic><topic>Stat3 protein</topic><topic>STAT3/NF-kB</topic><topic>Tumors</topic><topic>Western blotting</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zuo, Chaohui</creatorcontrib><creatorcontrib>Hong, Yuan</creatorcontrib><creatorcontrib>Qiu, Xiaoxin</creatorcontrib><creatorcontrib>Yang, Darong</creatorcontrib><creatorcontrib>Liu, Nianli</creatorcontrib><creatorcontrib>Sheng, Xinyi</creatorcontrib><creatorcontrib>Zhou, Kunyan</creatorcontrib><creatorcontrib>Tang, Bo</creatorcontrib><creatorcontrib>Xiong, Shuhan</creatorcontrib><creatorcontrib>Ma, Min</creatorcontrib><creatorcontrib>Liu, Zhuo</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zuo, Chaohui</au><au>Hong, Yuan</au><au>Qiu, Xiaoxin</au><au>Yang, Darong</au><au>Liu, Nianli</au><au>Sheng, Xinyi</au><au>Zhou, Kunyan</au><au>Tang, Bo</au><au>Xiong, Shuhan</au><au>Ma, Min</au><au>Liu, Zhuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Celecoxib suppresses proliferation and metastasis of pancreatic cancer cells by down-regulating STAT3 / NF-kB and L1CAM activities</atitle><jtitle>Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]</jtitle><addtitle>Pancreatology</addtitle><date>2018-04</date><risdate>2018</risdate><volume>18</volume><issue>3</issue><spage>328</spage><epage>333</epage><pages>328-333</pages><issn>1424-3903</issn><eissn>1424-3911</eissn><abstract>To explore the molecular mechanisms of celecoxib-induced pancreatic cancer suppression in vivo and in vitro.
The anti-pancreatic cancer activities of celecoxib (0, 20, 60 and 100 μmol/L) were investigated by cell viability and migration of Panc-1 and Bxpc-3 cells in vitro. The expression of L1CAM in pancreatic cancer and adjacent tissues was compared using immunohistochemistry. The expressions of L1CAM, STAT3, p-STAT3, NF-κB, p-NF-κB were determined by western blotting, and cell invasive ability was determined by wound healing assay in L1CAM-silenced and over-expressed Panc-1and Bxpc-3 cells.
The expression of L1CAM in pancreatic carcinoma was stronger than that in the adjacent tissues and L1CAM could increase the growth and invasion of pancreatic cancer cells. Over-expression of L1CAM activated the STAT3/NF-κB signaling pathway in Panc-1 and Bxpc-3 pancreatic cancer cells and celecoxib inhibited their viability and the expressions of STAT3, p-STAT3, NF-κB, p-NF-κB as well as full length L1CAM in a concentration dependent manner.
L1CAM was highly expressed in pancreatic cancer tissue and positively correlated with age, TNM staging and tumor differentiation. L1CAM activated the STAT/NF-κB signaling pathway and celecoxib could inhibit the activity of L1CAM, STAT3 and the NF-κB signaling pathway resulting in decreased growth and invasion of pancreatic cancer cells.</abstract><cop>Switzerland</cop><pub>Elsevier B.V</pub><pmid>29525378</pmid><doi>10.1016/j.pan.2018.02.006</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-0835-7464</orcidid></addata></record> |
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| identifier | ISSN: 1424-3903 |
| ispartof | Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2018-04, Vol.18 (3), p.328-333 |
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| source | Alma/SFX Local Collection |
| subjects | Angiogenesis Cancer therapies Celecoxib Cell adhesion & migration Cell migration Cell proliferation Chemotherapy Immunoglobulins Immunohistochemistry Invasiveness L1CAM Medical research Membranes Metastases Metastasis Molecular modelling Mortality NF-κB protein Overexpression Pancreatic cancer Pancreatic carcinoma Signal transduction Stat3 protein STAT3/NF-kB Tumors Western blotting Wound healing |
| title | Celecoxib suppresses proliferation and metastasis of pancreatic cancer cells by down-regulating STAT3 / NF-kB and L1CAM activities |
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