S100A4 promotes pancreatic cancer progression through a dual signaling pathway mediated by Src and focal adhesion kinase
S100A4 expression is associated with poor clinical outcomes of patients with pancreatic cancer. The effects of loss or gain of S100A4 were examined in pancreatic cancer cell lines. S100A4 downregulation remarkably reduces cell migration and invasion, inhibits proliferation and induces apoptosis in p...
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| Veröffentlicht in: | Scientific reports 2015-02, Vol.5 (1), p.8453-8453, Article 8453 |
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| creator | Che, Pulin Yang, Youfeng Han, Xiaosi Hu, Meng Sellers, Jeffery C. Londono-Joshi, Angelina I. Cai, Guo-Qiang Buchsbaum, Donald J. Christein, John D. Tang, Qinjiu Chen, Dongquan Li, Qianjun Grizzle, William E. Lu, Yin Ying Ding, Qiang |
| description | S100A4 expression is associated with poor clinical outcomes of patients with pancreatic cancer. The effects of loss or gain of S100A4 were examined in pancreatic cancer cell lines. S100A4 downregulation remarkably reduces cell migration and invasion, inhibits proliferation and induces apoptosis in pancreatic tumor cells. S100A4 downregulation results in significant cell growth inhibition and apoptosis in response to TGF-β1, supporting a non-canonical role of S100A4 in pancreatic cancer. The role of S100A4 in tumor progression was studied by using an orthotopic human pancreatic cancer xenograft mouse model. Tumor mass is remarkably decreased in animals injected with S100A4-deficient pancreatic tumor cells. P27
Kip1
expression and cleaved caspase-3 are increased, while cyclin E expression is decreased, in S100A4-deficient pancreatic tumors
in vivo
. S100A4-deficient tumors have lower expression of vascular endothelial growth factor, suggesting reduced angiogenesis. Biochemical assays revealed that S100A4 activates Src and focal adhesion kinase (FAK) signaling events and inhibition of both kinases is required to maximally block the tumorigenic potential of pancreatic cancer cells. These findings support that S100A4 plays an important role in pancreatic cancer progression
in vivo
and S100A4 promotes tumorigenic phenotypes of pancreatic cancer cells through the Src-FAK mediated dual signaling pathway. |
| doi_str_mv | 10.1038/srep08453 |
| format | Article |
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Kip1
expression and cleaved caspase-3 are increased, while cyclin E expression is decreased, in S100A4-deficient pancreatic tumors
in vivo
. S100A4-deficient tumors have lower expression of vascular endothelial growth factor, suggesting reduced angiogenesis. Biochemical assays revealed that S100A4 activates Src and focal adhesion kinase (FAK) signaling events and inhibition of both kinases is required to maximally block the tumorigenic potential of pancreatic cancer cells. These findings support that S100A4 plays an important role in pancreatic cancer progression
in vivo
and S100A4 promotes tumorigenic phenotypes of pancreatic cancer cells through the Src-FAK mediated dual signaling pathway.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep08453</identifier><identifier>PMID: 25677816</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/89 ; 631/67/1504/1713 ; 631/80/86/2366 ; 64/60 ; 96/63 ; Adhesion ; Angiogenesis ; Animals ; Apoptosis ; Caspase ; Caspase 3 - metabolism ; Caspase-3 ; Cell adhesion & migration ; Cell Line, Tumor ; Cell migration ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Cyclin E ; Cyclin E - metabolism ; Cyclin-dependent kinase inhibitor p27 ; Cyclin-Dependent Kinase Inhibitor p27 - metabolism ; Down-Regulation ; Female ; Focal adhesion kinase ; Focal Adhesion Protein-Tyrosine Kinases - metabolism ; Humanities and Social Sciences ; Humans ; Mice ; Mice, SCID ; multidisciplinary ; Pancreatic cancer ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; S100 Calcium-Binding Protein A4 ; S100 Proteins - antagonists & inhibitors ; S100 Proteins - genetics ; S100 Proteins - metabolism ; S100A4 protein ; Science ; Signal Transduction ; Src protein ; src-Family Kinases - metabolism ; Transforming Growth Factor beta1 - pharmacology ; Transforming growth factor-b1 ; Transplantation, Heterologous ; Tumor cell lines ; Tumor cells ; Tumors ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - metabolism ; Xenografts</subject><ispartof>Scientific reports, 2015-02, Vol.5 (1), p.8453-8453, Article 8453</ispartof><rights>The Author(s) 2015</rights><rights>Copyright Nature Publishing Group Feb 2015</rights><rights>Copyright © 2015, Macmillan Publishers Limited. All rights reserved 2015 Macmillan Publishers Limited. All rights reserved</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-f995634f7a766722afe6c8b66068122d37c5457d8dee0f8b83185fc945b50faa3</citedby><cites>FETCH-LOGICAL-c438t-f995634f7a766722afe6c8b66068122d37c5457d8dee0f8b83185fc945b50faa3</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/PMC4326725/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4326725/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,41099,42168,51555,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25677816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Che, Pulin</creatorcontrib><creatorcontrib>Yang, Youfeng</creatorcontrib><creatorcontrib>Han, Xiaosi</creatorcontrib><creatorcontrib>Hu, Meng</creatorcontrib><creatorcontrib>Sellers, Jeffery C.</creatorcontrib><creatorcontrib>Londono-Joshi, Angelina I.</creatorcontrib><creatorcontrib>Cai, Guo-Qiang</creatorcontrib><creatorcontrib>Buchsbaum, Donald J.</creatorcontrib><creatorcontrib>Christein, John D.</creatorcontrib><creatorcontrib>Tang, Qinjiu</creatorcontrib><creatorcontrib>Chen, Dongquan</creatorcontrib><creatorcontrib>Li, Qianjun</creatorcontrib><creatorcontrib>Grizzle, William E.</creatorcontrib><creatorcontrib>Lu, Yin Ying</creatorcontrib><creatorcontrib>Ding, Qiang</creatorcontrib><title>S100A4 promotes pancreatic cancer progression through a dual signaling pathway mediated by Src and focal adhesion kinase</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>S100A4 expression is associated with poor clinical outcomes of patients with pancreatic cancer. The effects of loss or gain of S100A4 were examined in pancreatic cancer cell lines. S100A4 downregulation remarkably reduces cell migration and invasion, inhibits proliferation and induces apoptosis in pancreatic tumor cells. S100A4 downregulation results in significant cell growth inhibition and apoptosis in response to TGF-β1, supporting a non-canonical role of S100A4 in pancreatic cancer. The role of S100A4 in tumor progression was studied by using an orthotopic human pancreatic cancer xenograft mouse model. Tumor mass is remarkably decreased in animals injected with S100A4-deficient pancreatic tumor cells. P27
Kip1
expression and cleaved caspase-3 are increased, while cyclin E expression is decreased, in S100A4-deficient pancreatic tumors
in vivo
. S100A4-deficient tumors have lower expression of vascular endothelial growth factor, suggesting reduced angiogenesis. Biochemical assays revealed that S100A4 activates Src and focal adhesion kinase (FAK) signaling events and inhibition of both kinases is required to maximally block the tumorigenic potential of pancreatic cancer cells. These findings support that S100A4 plays an important role in pancreatic cancer progression
in vivo
and S100A4 promotes tumorigenic phenotypes of pancreatic cancer cells through the Src-FAK mediated dual signaling pathway.</description><subject>13/89</subject><subject>631/67/1504/1713</subject><subject>631/80/86/2366</subject><subject>64/60</subject><subject>96/63</subject><subject>Adhesion</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Caspase</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cyclin E</subject><subject>Cyclin E - metabolism</subject><subject>Cyclin-dependent kinase inhibitor p27</subject><subject>Cyclin-Dependent Kinase Inhibitor p27 - metabolism</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Focal adhesion kinase</subject><subject>Focal Adhesion Protein-Tyrosine Kinases - metabolism</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>multidisciplinary</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>S100 Calcium-Binding Protein A4</subject><subject>S100 Proteins - antagonists & inhibitors</subject><subject>S100 Proteins - genetics</subject><subject>S100 Proteins - metabolism</subject><subject>S100A4 protein</subject><subject>Science</subject><subject>Signal Transduction</subject><subject>Src protein</subject><subject>src-Family Kinases - metabolism</subject><subject>Transforming Growth Factor beta1 - pharmacology</subject><subject>Transforming growth factor-b1</subject><subject>Transplantation, Heterologous</subject><subject>Tumor cell lines</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Xenografts</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkU1v1DAQhi0EotXSA38AWeICSEv9HeeCVFXlQ6rUQ8vZmjhO4pK1g52U7r_H7ZbVAr7MSO_jd0bzIvSako-UcH2ak5uIFpI_Q8eMCLlmnLHnB_0ROsn5lpQnWS1o_RIdMamqSlN1jO6vKSFnAk8pbuLsMp4g2ORg9hbb0rr0IPXJ5exjwPOQ4tIPGHC7wIiz7wOMPvTl2zz8gi3euNbD7FrcbPF1shhCi7toCwvt4B49fvgA2b1CLzoYszt5qiv0_fPFzfnX9eXVl2_nZ5drK7ie111dS8VFV0GlVMUYdE5Z3ShFlKaMtbyyUsiq1a1zpNON5lTLztZCNpJ0AHyFPu18p6Upy1kX5gSjmZLfQNqaCN78rQQ_mD7eGcFZGSiLwbsngxR_Li7PZuOzdeMIwcUlG6qkKqeuGS_o23_Q27ikcqFC6VrTElPBVuj9jrIp5pJet1-GEvMQqdlHWtg3h9vvyT8BFuDDDshFCr1LByP_c_sNgcKrxQ</recordid><startdate>20150213</startdate><enddate>20150213</enddate><creator>Che, Pulin</creator><creator>Yang, Youfeng</creator><creator>Han, Xiaosi</creator><creator>Hu, Meng</creator><creator>Sellers, Jeffery C.</creator><creator>Londono-Joshi, Angelina I.</creator><creator>Cai, Guo-Qiang</creator><creator>Buchsbaum, Donald J.</creator><creator>Christein, John D.</creator><creator>Tang, Qinjiu</creator><creator>Chen, Dongquan</creator><creator>Li, Qianjun</creator><creator>Grizzle, William E.</creator><creator>Lu, Yin Ying</creator><creator>Ding, Qiang</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150213</creationdate><title>S100A4 promotes pancreatic cancer progression through a dual signaling pathway mediated by Src and focal adhesion kinase</title><author>Che, Pulin ; Yang, Youfeng ; Han, Xiaosi ; Hu, Meng ; Sellers, Jeffery C. ; Londono-Joshi, Angelina I. ; Cai, Guo-Qiang ; Buchsbaum, Donald J. ; Christein, John D. ; Tang, Qinjiu ; Chen, Dongquan ; Li, Qianjun ; Grizzle, William E. ; Lu, Yin Ying ; Ding, Qiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-f995634f7a766722afe6c8b66068122d37c5457d8dee0f8b83185fc945b50faa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>13/89</topic><topic>631/67/1504/1713</topic><topic>631/80/86/2366</topic><topic>64/60</topic><topic>96/63</topic><topic>Adhesion</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Caspase</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase-3</topic><topic>Cell adhesion & migration</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cyclin E</topic><topic>Cyclin E - metabolism</topic><topic>Cyclin-dependent kinase inhibitor p27</topic><topic>Cyclin-Dependent Kinase Inhibitor p27 - metabolism</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Focal adhesion kinase</topic><topic>Focal Adhesion Protein-Tyrosine Kinases - metabolism</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>multidisciplinary</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>S100 Calcium-Binding Protein A4</topic><topic>S100 Proteins - antagonists & inhibitors</topic><topic>S100 Proteins - genetics</topic><topic>S100 Proteins - metabolism</topic><topic>S100A4 protein</topic><topic>Science</topic><topic>Signal Transduction</topic><topic>Src protein</topic><topic>src-Family Kinases - metabolism</topic><topic>Transforming Growth Factor beta1 - pharmacology</topic><topic>Transforming growth factor-b1</topic><topic>Transplantation, Heterologous</topic><topic>Tumor cell lines</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Che, Pulin</creatorcontrib><creatorcontrib>Yang, Youfeng</creatorcontrib><creatorcontrib>Han, Xiaosi</creatorcontrib><creatorcontrib>Hu, Meng</creatorcontrib><creatorcontrib>Sellers, Jeffery C.</creatorcontrib><creatorcontrib>Londono-Joshi, Angelina I.</creatorcontrib><creatorcontrib>Cai, Guo-Qiang</creatorcontrib><creatorcontrib>Buchsbaum, Donald J.</creatorcontrib><creatorcontrib>Christein, John D.</creatorcontrib><creatorcontrib>Tang, Qinjiu</creatorcontrib><creatorcontrib>Chen, Dongquan</creatorcontrib><creatorcontrib>Li, Qianjun</creatorcontrib><creatorcontrib>Grizzle, William E.</creatorcontrib><creatorcontrib>Lu, Yin Ying</creatorcontrib><creatorcontrib>Ding, Qiang</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Che, Pulin</au><au>Yang, Youfeng</au><au>Han, Xiaosi</au><au>Hu, Meng</au><au>Sellers, Jeffery C.</au><au>Londono-Joshi, Angelina I.</au><au>Cai, Guo-Qiang</au><au>Buchsbaum, Donald J.</au><au>Christein, John D.</au><au>Tang, Qinjiu</au><au>Chen, Dongquan</au><au>Li, Qianjun</au><au>Grizzle, William E.</au><au>Lu, Yin Ying</au><au>Ding, Qiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>S100A4 promotes pancreatic cancer progression through a dual signaling pathway mediated by Src and focal adhesion kinase</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2015-02-13</date><risdate>2015</risdate><volume>5</volume><issue>1</issue><spage>8453</spage><epage>8453</epage><pages>8453-8453</pages><artnum>8453</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>S100A4 expression is associated with poor clinical outcomes of patients with pancreatic cancer. The effects of loss or gain of S100A4 were examined in pancreatic cancer cell lines. S100A4 downregulation remarkably reduces cell migration and invasion, inhibits proliferation and induces apoptosis in pancreatic tumor cells. S100A4 downregulation results in significant cell growth inhibition and apoptosis in response to TGF-β1, supporting a non-canonical role of S100A4 in pancreatic cancer. The role of S100A4 in tumor progression was studied by using an orthotopic human pancreatic cancer xenograft mouse model. Tumor mass is remarkably decreased in animals injected with S100A4-deficient pancreatic tumor cells. P27
Kip1
expression and cleaved caspase-3 are increased, while cyclin E expression is decreased, in S100A4-deficient pancreatic tumors
in vivo
. S100A4-deficient tumors have lower expression of vascular endothelial growth factor, suggesting reduced angiogenesis. Biochemical assays revealed that S100A4 activates Src and focal adhesion kinase (FAK) signaling events and inhibition of both kinases is required to maximally block the tumorigenic potential of pancreatic cancer cells. These findings support that S100A4 plays an important role in pancreatic cancer progression
in vivo
and S100A4 promotes tumorigenic phenotypes of pancreatic cancer cells through the Src-FAK mediated dual signaling pathway.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25677816</pmid><doi>10.1038/srep08453</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 13/89 631/67/1504/1713 631/80/86/2366 64/60 96/63 Adhesion Angiogenesis Animals Apoptosis Caspase Caspase 3 - metabolism Caspase-3 Cell adhesion & migration Cell Line, Tumor Cell migration Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Cyclin E Cyclin E - metabolism Cyclin-dependent kinase inhibitor p27 Cyclin-Dependent Kinase Inhibitor p27 - metabolism Down-Regulation Female Focal adhesion kinase Focal Adhesion Protein-Tyrosine Kinases - metabolism Humanities and Social Sciences Humans Mice Mice, SCID multidisciplinary Pancreatic cancer Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology S100 Calcium-Binding Protein A4 S100 Proteins - antagonists & inhibitors S100 Proteins - genetics S100 Proteins - metabolism S100A4 protein Science Signal Transduction Src protein src-Family Kinases - metabolism Transforming Growth Factor beta1 - pharmacology Transforming growth factor-b1 Transplantation, Heterologous Tumor cell lines Tumor cells Tumors Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism Xenografts |
| title | S100A4 promotes pancreatic cancer progression through a dual signaling pathway mediated by Src and focal adhesion kinase |
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