IL-22 produced by cancer-associated fibroblasts promotes gastric cancer cell invasion via STAT3 and ERK signaling
Background: Interleukin-22 (IL-22) has been recently highlighted owing to its biological significance in the modulation of tissue responses during inflammation. However, the role of IL-22 in carcinogenesis has remained unclear. Here, we investigated the pathophysiological significance of IL-22 expre...
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| Veröffentlicht in: | British journal of cancer 2014-08, Vol.111 (4), p.763-771 |
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| container_title | British journal of cancer |
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| creator | Fukui, H Zhang, X Sun, C Hara, K Kikuchi, S Yamasaki, T Kondo, T Tomita, T Oshima, T Watari, J Imura, J Fujimori, T Sasako, M Miwa, H |
| description | Background:
Interleukin-22 (IL-22) has been recently highlighted owing to its biological significance in the modulation of tissue responses during inflammation. However, the role of IL-22 in carcinogenesis has remained unclear. Here, we investigated the pathophysiological significance of IL-22 expression in gastric cancer tissues and examined the mechanism by which IL-22 promotes gastric cancer cell invasion.
Methods:
Human gastric cancer specimens were analysed by immunohistochemistry for expression of IL-22 and IL-22 receptor 1 (IL-22R1). The effects of IL-22-induced STAT3 and ERK signalling on invasive ability of gastric cancer cells were examined using a small-interfering RNA system and specific inhibitors. AGS cells were co-cultured with cancer-associated fibroblasts (CAFs) from human gastric cancer tissues and assessed by invasion assay.
Results:
Interleukin-22 and its receptor were expressed in
α
-smooth muscle actin-positive stromal cells and tumour cells at the invasive front of gastric cancer tissues, respectively. The expression of IL-22 and IL-22R1 was significantly related to lymphatic invasion. Interleukin-22 treatment promoted the invasive ability of gastric cancer cells through STAT3 and ERK activation. The invasive ability of gastric cancer cells was significantly enhanced by co-culture with IL-22-expressing CAFs.
Conclusions:
Interleukin-22 produced by CAFs promotes gastric cancer cell invasion via STAT3 and ERK signalling. |
| doi_str_mv | 10.1038/bjc.2014.336 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4134496</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3400651451</sourcerecordid><originalsourceid>FETCH-LOGICAL-c616t-3214e7e105823b4a6e1b3dda5d09a370ca3a30039cf9ed9add36b4557b678ee53</originalsourceid><addsrcrecordid>eNptkV2LEzEUhoMobl2981oC4p1T8zXJzI2wLKsuFgSt1-HkY8aUadJNpoX996a0rit4FU7Ow3tO8iD0mpIlJbz7YDZ2yQgVS87lE7SgLWcN7Zh6ihaEENWQnpEL9KKUTS170qnn6IKJniup6ALd3a4axvAuJ7e33mFzjy1E63MDpSQbYK6XQzA5mQnKXI7kNs2-4LGWOdgzjq2fJhziAUpIER8C4B_rqzXHEB2--f4VlzBGmEIcX6JnA0zFvzqfl-jnp5v19Zdm9e3z7fXVqrGSyrnhjAqvPCVtx7gRID013DloHemBK2KBAyeE93bovevBOS6NaFtlpOq8b_kl-njK3e3N1jvr45xh0rsctpDvdYKg_-3E8EuP6aAF5UL0sga8PQfkdLf3ZdabtM_1EUXTtmUdbykTlXp_omxOpWQ_PEygRB8F6SpIHwXpKqjibx5v9QD_MVKBd2cAioVpyPV7Q_nLdYoxIo9cc-JKbcXR50fb_W_wby5CqHw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1552835124</pqid></control><display><type>article</type><title>IL-22 produced by cancer-associated fibroblasts promotes gastric cancer cell invasion via STAT3 and ERK signaling</title><source>Open Access: PubMed Central</source><source>MEDLINE</source><source>Springer Nature - Connect here FIRST to enable access</source><source>SpringerLink (Online service)</source><source>EZB Electronic Journals Library</source><creator>Fukui, H ; Zhang, X ; Sun, C ; Hara, K ; Kikuchi, S ; Yamasaki, T ; Kondo, T ; Tomita, T ; Oshima, T ; Watari, J ; Imura, J ; Fujimori, T ; Sasako, M ; Miwa, H</creator><creatorcontrib>Fukui, H ; Zhang, X ; Sun, C ; Hara, K ; Kikuchi, S ; Yamasaki, T ; Kondo, T ; Tomita, T ; Oshima, T ; Watari, J ; Imura, J ; Fujimori, T ; Sasako, M ; Miwa, H</creatorcontrib><description>Background:
Interleukin-22 (IL-22) has been recently highlighted owing to its biological significance in the modulation of tissue responses during inflammation. However, the role of IL-22 in carcinogenesis has remained unclear. Here, we investigated the pathophysiological significance of IL-22 expression in gastric cancer tissues and examined the mechanism by which IL-22 promotes gastric cancer cell invasion.
Methods:
Human gastric cancer specimens were analysed by immunohistochemistry for expression of IL-22 and IL-22 receptor 1 (IL-22R1). The effects of IL-22-induced STAT3 and ERK signalling on invasive ability of gastric cancer cells were examined using a small-interfering RNA system and specific inhibitors. AGS cells were co-cultured with cancer-associated fibroblasts (CAFs) from human gastric cancer tissues and assessed by invasion assay.
Results:
Interleukin-22 and its receptor were expressed in
α
-smooth muscle actin-positive stromal cells and tumour cells at the invasive front of gastric cancer tissues, respectively. The expression of IL-22 and IL-22R1 was significantly related to lymphatic invasion. Interleukin-22 treatment promoted the invasive ability of gastric cancer cells through STAT3 and ERK activation. The invasive ability of gastric cancer cells was significantly enhanced by co-culture with IL-22-expressing CAFs.
Conclusions:
Interleukin-22 produced by CAFs promotes gastric cancer cell invasion via STAT3 and ERK signalling.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/bjc.2014.336</identifier><identifier>PMID: 24937671</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/1504/1829 ; 631/67/322 ; 631/80/84/2336 ; 631/80/86 ; Adult ; Aged ; Aged, 80 and over ; Antibodies ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell Line, Tumor ; Cells ; Coculture Techniques ; Cytokines ; Drug Resistance ; Epidemiology ; Female ; Fibroblasts ; Fibroblasts - metabolism ; Gastric cancer ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Inflammation ; Interleukin-22 ; Interleukins - metabolism ; Internal medicine ; Male ; MAP Kinase Signaling System ; Medical sciences ; Medicine ; Metastasis ; Middle Aged ; Molecular Diagnostics ; Molecular Medicine ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Neoplasm Invasiveness ; Oncology ; Phosphorylation ; Protein Processing, Post-Translational ; Receptors, Interleukin - metabolism ; STAT3 Transcription Factor - metabolism ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors</subject><ispartof>British journal of cancer, 2014-08, Vol.111 (4), p.763-771</ispartof><rights>The Author(s) 2014</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Aug 12, 2014</rights><rights>Copyright © 2014 Cancer Research UK 2014 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c616t-3214e7e105823b4a6e1b3dda5d09a370ca3a30039cf9ed9add36b4557b678ee53</citedby><cites>FETCH-LOGICAL-c616t-3214e7e105823b4a6e1b3dda5d09a370ca3a30039cf9ed9add36b4557b678ee53</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/PMC4134496/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134496/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28722061$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24937671$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fukui, H</creatorcontrib><creatorcontrib>Zhang, X</creatorcontrib><creatorcontrib>Sun, C</creatorcontrib><creatorcontrib>Hara, K</creatorcontrib><creatorcontrib>Kikuchi, S</creatorcontrib><creatorcontrib>Yamasaki, T</creatorcontrib><creatorcontrib>Kondo, T</creatorcontrib><creatorcontrib>Tomita, T</creatorcontrib><creatorcontrib>Oshima, T</creatorcontrib><creatorcontrib>Watari, J</creatorcontrib><creatorcontrib>Imura, J</creatorcontrib><creatorcontrib>Fujimori, T</creatorcontrib><creatorcontrib>Sasako, M</creatorcontrib><creatorcontrib>Miwa, H</creatorcontrib><title>IL-22 produced by cancer-associated fibroblasts promotes gastric cancer cell invasion via STAT3 and ERK signaling</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Background:
Interleukin-22 (IL-22) has been recently highlighted owing to its biological significance in the modulation of tissue responses during inflammation. However, the role of IL-22 in carcinogenesis has remained unclear. Here, we investigated the pathophysiological significance of IL-22 expression in gastric cancer tissues and examined the mechanism by which IL-22 promotes gastric cancer cell invasion.
Methods:
Human gastric cancer specimens were analysed by immunohistochemistry for expression of IL-22 and IL-22 receptor 1 (IL-22R1). The effects of IL-22-induced STAT3 and ERK signalling on invasive ability of gastric cancer cells were examined using a small-interfering RNA system and specific inhibitors. AGS cells were co-cultured with cancer-associated fibroblasts (CAFs) from human gastric cancer tissues and assessed by invasion assay.
Results:
Interleukin-22 and its receptor were expressed in
α
-smooth muscle actin-positive stromal cells and tumour cells at the invasive front of gastric cancer tissues, respectively. The expression of IL-22 and IL-22R1 was significantly related to lymphatic invasion. Interleukin-22 treatment promoted the invasive ability of gastric cancer cells through STAT3 and ERK activation. The invasive ability of gastric cancer cells was significantly enhanced by co-culture with IL-22-expressing CAFs.
Conclusions:
Interleukin-22 produced by CAFs promotes gastric cancer cell invasion via STAT3 and ERK signalling.</description><subject>631/67/1504/1829</subject><subject>631/67/322</subject><subject>631/80/84/2336</subject><subject>631/80/86</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antibodies</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell Line, Tumor</subject><subject>Cells</subject><subject>Coculture Techniques</subject><subject>Cytokines</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Gastric cancer</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin-22</subject><subject>Interleukins - metabolism</subject><subject>Internal medicine</subject><subject>Male</subject><subject>MAP Kinase Signaling System</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Molecular Diagnostics</subject><subject>Molecular Medicine</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Neoplasm Invasiveness</subject><subject>Oncology</subject><subject>Phosphorylation</subject><subject>Protein Processing, Post-Translational</subject><subject>Receptors, Interleukin - metabolism</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin-22</topic><topic>Interleukins - metabolism</topic><topic>Internal medicine</topic><topic>Male</topic><topic>MAP Kinase Signaling System</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Molecular Diagnostics</topic><topic>Molecular Medicine</topic><topic>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</topic><topic>Neoplasm Invasiveness</topic><topic>Oncology</topic><topic>Phosphorylation</topic><topic>Protein Processing, Post-Translational</topic><topic>Receptors, Interleukin - metabolism</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fukui, H</creatorcontrib><creatorcontrib>Zhang, X</creatorcontrib><creatorcontrib>Sun, C</creatorcontrib><creatorcontrib>Hara, K</creatorcontrib><creatorcontrib>Kikuchi, S</creatorcontrib><creatorcontrib>Yamasaki, T</creatorcontrib><creatorcontrib>Kondo, T</creatorcontrib><creatorcontrib>Tomita, T</creatorcontrib><creatorcontrib>Oshima, T</creatorcontrib><creatorcontrib>Watari, J</creatorcontrib><creatorcontrib>Imura, J</creatorcontrib><creatorcontrib>Fujimori, T</creatorcontrib><creatorcontrib>Sasako, M</creatorcontrib><creatorcontrib>Miwa, H</creatorcontrib><collection>Springer_OA刊</collection><collection>Pascal-Francis</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>Proquest Nursing & Allied Health Source</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (Proquest)</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)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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 China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fukui, H</au><au>Zhang, X</au><au>Sun, C</au><au>Hara, K</au><au>Kikuchi, S</au><au>Yamasaki, T</au><au>Kondo, T</au><au>Tomita, T</au><au>Oshima, T</au><au>Watari, J</au><au>Imura, J</au><au>Fujimori, T</au><au>Sasako, M</au><au>Miwa, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-22 produced by cancer-associated fibroblasts promotes gastric cancer cell invasion via STAT3 and ERK signaling</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2014-08-12</date><risdate>2014</risdate><volume>111</volume><issue>4</issue><spage>763</spage><epage>771</epage><pages>763-771</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Background:
Interleukin-22 (IL-22) has been recently highlighted owing to its biological significance in the modulation of tissue responses during inflammation. However, the role of IL-22 in carcinogenesis has remained unclear. Here, we investigated the pathophysiological significance of IL-22 expression in gastric cancer tissues and examined the mechanism by which IL-22 promotes gastric cancer cell invasion.
Methods:
Human gastric cancer specimens were analysed by immunohistochemistry for expression of IL-22 and IL-22 receptor 1 (IL-22R1). The effects of IL-22-induced STAT3 and ERK signalling on invasive ability of gastric cancer cells were examined using a small-interfering RNA system and specific inhibitors. AGS cells were co-cultured with cancer-associated fibroblasts (CAFs) from human gastric cancer tissues and assessed by invasion assay.
Results:
Interleukin-22 and its receptor were expressed in
α
-smooth muscle actin-positive stromal cells and tumour cells at the invasive front of gastric cancer tissues, respectively. The expression of IL-22 and IL-22R1 was significantly related to lymphatic invasion. Interleukin-22 treatment promoted the invasive ability of gastric cancer cells through STAT3 and ERK activation. The invasive ability of gastric cancer cells was significantly enhanced by co-culture with IL-22-expressing CAFs.
Conclusions:
Interleukin-22 produced by CAFs promotes gastric cancer cell invasion via STAT3 and ERK signalling.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24937671</pmid><doi>10.1038/bjc.2014.336</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | British journal of cancer, 2014-08, Vol.111 (4), p.763-771 |
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| subjects | 631/67/1504/1829 631/67/322 631/80/84/2336 631/80/86 Adult Aged Aged, 80 and over Antibodies Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Research Cell Line, Tumor Cells Coculture Techniques Cytokines Drug Resistance Epidemiology Female Fibroblasts Fibroblasts - metabolism Gastric cancer Gastroenterology. Liver. Pancreas. Abdomen Humans Inflammation Interleukin-22 Interleukins - metabolism Internal medicine Male MAP Kinase Signaling System Medical sciences Medicine Metastasis Middle Aged Molecular Diagnostics Molecular Medicine Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Neoplasm Invasiveness Oncology Phosphorylation Protein Processing, Post-Translational Receptors, Interleukin - metabolism STAT3 Transcription Factor - metabolism Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors |
| title | IL-22 produced by cancer-associated fibroblasts promotes gastric cancer cell invasion via STAT3 and ERK signaling |
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