Cancer cell-derived IL-1α promotes HGF secretion by stromal cells and enhances metastatic potential in pancreatic cancer cells
Background and Objectives Interleukin (IL)‐1α and hepatocyte growth factor (HGF) play an important role in pancreatic cancer proliferation, angiogenesis, and invasiveness. The aim of this study was to investigate the cooperative role of HGF and IL‐1α in metastatic processes promoted by interactions...
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| Veröffentlicht in: | Journal of surgical oncology 2010-10, Vol.102 (5), p.469-477 |
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| container_title | Journal of surgical oncology |
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| creator | Xu, Donghui Matsuo, Yoichi Ma, Jiachi Koide, Shuji Ochi, Nobuo Yasuda, Akira Funahashi, Hitoshi Okada, Yuji Takeyama, Hiromitsu |
| description | Background and Objectives
Interleukin (IL)‐1α and hepatocyte growth factor (HGF) play an important role in pancreatic cancer proliferation, angiogenesis, and invasiveness. The aim of this study was to investigate the cooperative role of HGF and IL‐1α in metastatic processes promoted by interactions between pancreatic cancer cells and stromal cells.
Methods
Expression of IL‐1α and HGF mRNA and protein was determined by RT‐PCR and ELISA. The effect of HGF on metastatic potential was evaluated by proliferation, invasion, and angiogenesis assays using an in vitro system consisting of co‐cultured tumor cells and stromal cells.
Results
IL‐1α expression was closely correlated with metastatic potential, and cancer cell‐derived IL‐1α significantly promoted HGF expression by fibroblasts (P |
| doi_str_mv | 10.1002/jso.21530 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_755400790</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>755400790</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3620-197e418b53a90cea3e12d347748e1d300a55aff0ee6612c44596c2b21b9c97203</originalsourceid><addsrcrecordid>eNp1kM1uEzEUhS0EoqGw4AWQd4jFtNd_43iJRm1aFFGVH3VpeTw3wmV-gu0AWfFMvAjPhJO0ZcXqSj7fOff6EPKSwQkD4Ke3aTrhTAl4RGYMTF0ZMPPHZFY0Xklt4Ig8S-kWAIyp5VNyxGGuuVEwI78aN3qM1GPfVx3G8B07erms2J_fdB2nYcqY6MXinCb0EXOYRtpuacpFcv3elagbO4rjl11QogNml7LLwdN1MY85FC6MdF3kiPt3_29lek6erFyf8MXdPCafz88-NRfV8mpx2bxdVl7UHCpmNEo2b5VwBjw6gYx3Qmot58g6AeCUcqsVINY1415KZWrPW85a443mII7J60Nu-dS3DaZsh5B2F7gRp02yWikJUKoq5JsD6eOUUsSVXccwuLi1DOyublvqtvu6C_vqLnXTDtg9kPf9FuD0APwIPW7_n2Tffby6j6wOjpAy_nxwuPjV1lpoZW_eL2zTXKsPN3Jpr8VfJ22Z3Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>755400790</pqid></control><display><type>article</type><title>Cancer cell-derived IL-1α promotes HGF secretion by stromal cells and enhances metastatic potential in pancreatic cancer cells</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><creator>Xu, Donghui ; Matsuo, Yoichi ; Ma, Jiachi ; Koide, Shuji ; Ochi, Nobuo ; Yasuda, Akira ; Funahashi, Hitoshi ; Okada, Yuji ; Takeyama, Hiromitsu</creator><creatorcontrib>Xu, Donghui ; Matsuo, Yoichi ; Ma, Jiachi ; Koide, Shuji ; Ochi, Nobuo ; Yasuda, Akira ; Funahashi, Hitoshi ; Okada, Yuji ; Takeyama, Hiromitsu</creatorcontrib><description>Background and Objectives
Interleukin (IL)‐1α and hepatocyte growth factor (HGF) play an important role in pancreatic cancer proliferation, angiogenesis, and invasiveness. The aim of this study was to investigate the cooperative role of HGF and IL‐1α in metastatic processes promoted by interactions between pancreatic cancer cells and stromal cells.
Methods
Expression of IL‐1α and HGF mRNA and protein was determined by RT‐PCR and ELISA. The effect of HGF on metastatic potential was evaluated by proliferation, invasion, and angiogenesis assays using an in vitro system consisting of co‐cultured tumor cells and stromal cells.
Results
IL‐1α expression was closely correlated with metastatic potential, and cancer cell‐derived IL‐1α significantly promoted HGF expression by fibroblasts (P < 0.01). HGF not only enhanced the invasiveness and proliferation of pancreatic cancer cells, but also enhanced migration and proliferation of human umbilical vein endothelial cells (HUVECs). HGF significantly enhanced HUVEC tube formation (P < 0.01). Furthermore, the high liver‐metastatic pancreatic cancer cell line (BxPC‐3), which secretes IL‐1α, significantly enhanced HUVEC tube formation compared with the low liver‐metastatic cell line (Capan‐2), which does not produce IL‐1α (P < 0.01).
Conclusion
Autocrine IL‐1α and paracrine HGF co‐enhance the metastatic potential of pancreatic cancer cells via both IL‐1α and HGF signaling pathways. J. Surg. Oncol. 2010;102:469–477. © 2010 Wiley‐Liss, Inc.</description><identifier>ISSN: 0022-4790</identifier><identifier>EISSN: 1096-9098</identifier><identifier>DOI: 10.1002/jso.21530</identifier><identifier>PMID: 20872950</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>angiogenesis ; Cell Communication ; Cell Line, Tumor ; Coculture Techniques ; Enzyme-Linked Immunosorbent Assay ; Hepatocyte Growth Factor - metabolism ; HGF ; Humans ; IL-1α ; Interleukin-1alpha - metabolism ; Neoplasm Metastasis ; Neoplasm Proteins - metabolism ; pancreatic cancer ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Signal Transduction ; Stromal Cells - secretion ; tumor-stromal interaction</subject><ispartof>Journal of surgical oncology, 2010-10, Vol.102 (5), p.469-477</ispartof><rights>Copyright © 2010 Wiley‐Liss, Inc.</rights><rights>J. Surg. Oncol. 2010;102:469-477. © 2010 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3620-197e418b53a90cea3e12d347748e1d300a55aff0ee6612c44596c2b21b9c97203</citedby><cites>FETCH-LOGICAL-c3620-197e418b53a90cea3e12d347748e1d300a55aff0ee6612c44596c2b21b9c97203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjso.21530$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjso.21530$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20872950$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Donghui</creatorcontrib><creatorcontrib>Matsuo, Yoichi</creatorcontrib><creatorcontrib>Ma, Jiachi</creatorcontrib><creatorcontrib>Koide, Shuji</creatorcontrib><creatorcontrib>Ochi, Nobuo</creatorcontrib><creatorcontrib>Yasuda, Akira</creatorcontrib><creatorcontrib>Funahashi, Hitoshi</creatorcontrib><creatorcontrib>Okada, Yuji</creatorcontrib><creatorcontrib>Takeyama, Hiromitsu</creatorcontrib><title>Cancer cell-derived IL-1α promotes HGF secretion by stromal cells and enhances metastatic potential in pancreatic cancer cells</title><title>Journal of surgical oncology</title><addtitle>J. Surg. Oncol</addtitle><description>Background and Objectives
Interleukin (IL)‐1α and hepatocyte growth factor (HGF) play an important role in pancreatic cancer proliferation, angiogenesis, and invasiveness. The aim of this study was to investigate the cooperative role of HGF and IL‐1α in metastatic processes promoted by interactions between pancreatic cancer cells and stromal cells.
Methods
Expression of IL‐1α and HGF mRNA and protein was determined by RT‐PCR and ELISA. The effect of HGF on metastatic potential was evaluated by proliferation, invasion, and angiogenesis assays using an in vitro system consisting of co‐cultured tumor cells and stromal cells.
Results
IL‐1α expression was closely correlated with metastatic potential, and cancer cell‐derived IL‐1α significantly promoted HGF expression by fibroblasts (P < 0.01). HGF not only enhanced the invasiveness and proliferation of pancreatic cancer cells, but also enhanced migration and proliferation of human umbilical vein endothelial cells (HUVECs). HGF significantly enhanced HUVEC tube formation (P < 0.01). Furthermore, the high liver‐metastatic pancreatic cancer cell line (BxPC‐3), which secretes IL‐1α, significantly enhanced HUVEC tube formation compared with the low liver‐metastatic cell line (Capan‐2), which does not produce IL‐1α (P < 0.01).
Conclusion
Autocrine IL‐1α and paracrine HGF co‐enhance the metastatic potential of pancreatic cancer cells via both IL‐1α and HGF signaling pathways. J. Surg. Oncol. 2010;102:469–477. © 2010 Wiley‐Liss, Inc.</description><subject>angiogenesis</subject><subject>Cell Communication</subject><subject>Cell Line, Tumor</subject><subject>Coculture Techniques</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Hepatocyte Growth Factor - metabolism</subject><subject>HGF</subject><subject>Humans</subject><subject>IL-1α</subject><subject>Interleukin-1alpha - metabolism</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasm Proteins - metabolism</subject><subject>pancreatic cancer</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction</subject><subject>Stromal Cells - secretion</subject><subject>tumor-stromal interaction</subject><issn>0022-4790</issn><issn>1096-9098</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM1uEzEUhS0EoqGw4AWQd4jFtNd_43iJRm1aFFGVH3VpeTw3wmV-gu0AWfFMvAjPhJO0ZcXqSj7fOff6EPKSwQkD4Ke3aTrhTAl4RGYMTF0ZMPPHZFY0Xklt4Ig8S-kWAIyp5VNyxGGuuVEwI78aN3qM1GPfVx3G8B07erms2J_fdB2nYcqY6MXinCb0EXOYRtpuacpFcv3elagbO4rjl11QogNml7LLwdN1MY85FC6MdF3kiPt3_29lek6erFyf8MXdPCafz88-NRfV8mpx2bxdVl7UHCpmNEo2b5VwBjw6gYx3Qmot58g6AeCUcqsVINY1415KZWrPW85a443mII7J60Nu-dS3DaZsh5B2F7gRp02yWikJUKoq5JsD6eOUUsSVXccwuLi1DOyublvqtvu6C_vqLnXTDtg9kPf9FuD0APwIPW7_n2Tffby6j6wOjpAy_nxwuPjV1lpoZW_eL2zTXKsPN3Jpr8VfJ22Z3Q</recordid><startdate>20101001</startdate><enddate>20101001</enddate><creator>Xu, Donghui</creator><creator>Matsuo, Yoichi</creator><creator>Ma, Jiachi</creator><creator>Koide, Shuji</creator><creator>Ochi, Nobuo</creator><creator>Yasuda, Akira</creator><creator>Funahashi, Hitoshi</creator><creator>Okada, Yuji</creator><creator>Takeyama, Hiromitsu</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>20101001</creationdate><title>Cancer cell-derived IL-1α promotes HGF secretion by stromal cells and enhances metastatic potential in pancreatic cancer cells</title><author>Xu, Donghui ; Matsuo, Yoichi ; Ma, Jiachi ; Koide, Shuji ; Ochi, Nobuo ; Yasuda, Akira ; Funahashi, Hitoshi ; Okada, Yuji ; Takeyama, Hiromitsu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3620-197e418b53a90cea3e12d347748e1d300a55aff0ee6612c44596c2b21b9c97203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>angiogenesis</topic><topic>Cell Communication</topic><topic>Cell Line, Tumor</topic><topic>Coculture Techniques</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Hepatocyte Growth Factor - metabolism</topic><topic>HGF</topic><topic>Humans</topic><topic>IL-1α</topic><topic>Interleukin-1alpha - metabolism</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasm Proteins - metabolism</topic><topic>pancreatic cancer</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction</topic><topic>Stromal Cells - secretion</topic><topic>tumor-stromal interaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Donghui</creatorcontrib><creatorcontrib>Matsuo, Yoichi</creatorcontrib><creatorcontrib>Ma, Jiachi</creatorcontrib><creatorcontrib>Koide, Shuji</creatorcontrib><creatorcontrib>Ochi, Nobuo</creatorcontrib><creatorcontrib>Yasuda, Akira</creatorcontrib><creatorcontrib>Funahashi, Hitoshi</creatorcontrib><creatorcontrib>Okada, Yuji</creatorcontrib><creatorcontrib>Takeyama, Hiromitsu</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>Journal of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Donghui</au><au>Matsuo, Yoichi</au><au>Ma, Jiachi</au><au>Koide, Shuji</au><au>Ochi, Nobuo</au><au>Yasuda, Akira</au><au>Funahashi, Hitoshi</au><au>Okada, Yuji</au><au>Takeyama, Hiromitsu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer cell-derived IL-1α promotes HGF secretion by stromal cells and enhances metastatic potential in pancreatic cancer cells</atitle><jtitle>Journal of surgical oncology</jtitle><addtitle>J. Surg. Oncol</addtitle><date>2010-10-01</date><risdate>2010</risdate><volume>102</volume><issue>5</issue><spage>469</spage><epage>477</epage><pages>469-477</pages><issn>0022-4790</issn><eissn>1096-9098</eissn><abstract>Background and Objectives
Interleukin (IL)‐1α and hepatocyte growth factor (HGF) play an important role in pancreatic cancer proliferation, angiogenesis, and invasiveness. The aim of this study was to investigate the cooperative role of HGF and IL‐1α in metastatic processes promoted by interactions between pancreatic cancer cells and stromal cells.
Methods
Expression of IL‐1α and HGF mRNA and protein was determined by RT‐PCR and ELISA. The effect of HGF on metastatic potential was evaluated by proliferation, invasion, and angiogenesis assays using an in vitro system consisting of co‐cultured tumor cells and stromal cells.
Results
IL‐1α expression was closely correlated with metastatic potential, and cancer cell‐derived IL‐1α significantly promoted HGF expression by fibroblasts (P < 0.01). HGF not only enhanced the invasiveness and proliferation of pancreatic cancer cells, but also enhanced migration and proliferation of human umbilical vein endothelial cells (HUVECs). HGF significantly enhanced HUVEC tube formation (P < 0.01). Furthermore, the high liver‐metastatic pancreatic cancer cell line (BxPC‐3), which secretes IL‐1α, significantly enhanced HUVEC tube formation compared with the low liver‐metastatic cell line (Capan‐2), which does not produce IL‐1α (P < 0.01).
Conclusion
Autocrine IL‐1α and paracrine HGF co‐enhance the metastatic potential of pancreatic cancer cells via both IL‐1α and HGF signaling pathways. J. Surg. Oncol. 2010;102:469–477. © 2010 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20872950</pmid><doi>10.1002/jso.21530</doi><tpages>9</tpages></addata></record> |
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| subjects | angiogenesis Cell Communication Cell Line, Tumor Coculture Techniques Enzyme-Linked Immunosorbent Assay Hepatocyte Growth Factor - metabolism HGF Humans IL-1α Interleukin-1alpha - metabolism Neoplasm Metastasis Neoplasm Proteins - metabolism pancreatic cancer Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Polymerase Chain Reaction RNA, Messenger - metabolism Signal Transduction Stromal Cells - secretion tumor-stromal interaction |
| title | Cancer cell-derived IL-1α promotes HGF secretion by stromal cells and enhances metastatic potential in pancreatic cancer cells |
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