Tumor-neuroglia interaction promotes pancreatic cancer metastasis
: The peripheral nervous system (PNS) plays an important role in tumor growth and progression. Schwann cells (SCs), the main glia cells of the PNS, augment cancer metastasis in contact-dependent or contact-independent manner in various malignancies. In the present study, we aimed to determine whethe...
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| Veröffentlicht in: | Theranostics 2020-01, Vol.10 (11), p.5029-5047 |
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| creator | Su, Dan Guo, Xiaofeng Huang, Leyi Ye, Huilin Li, Zhiguo Lin, Longfa Chen, Rufu Zhou, Quanbo |
| description | : The peripheral nervous system (PNS) plays an important role in tumor growth and progression. Schwann cells (SCs), the main glia cells of the PNS, augment cancer metastasis in contact-dependent or contact-independent manner in various malignancies. In the present study, we aimed to determine whether interplay between pancreatic cancer cells and SCs via paracrine signaling contributes to cancer progression.
: Immunofluorescence analysis was performed to reveal the distribution of SCs in PDAC tissues and to determine the prognostic value and clinicopathological relevance of the level of intra‑tumoral SC markers for patients diagnosed with PDAC. Transwell assays and wound healing assays were carried out to investigate the influence of SC conditioned medium (SCM), SC co‑culture, or co-cultured CM on the migratory and invasive abilities of pancreatic cancer cells. The mechanism of SCs induced cancer cells migration and invasion was confirmed using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assays (ELISAs), western blotting, immunofluorescence, immunohistochemistry, siRNA-mediated gene interference, and an
mouse model.
: Immunofluorescence analysis of tissue samples revealed that there were two different types of SCs distributed in the tumor microenvironment, the presence of which correlated with several clinicopathological characteristics and overall survival for patients with PDAC. Although SCM had no impact on the motility and invasiveness of tumor cells, both co-cultivation with SCs and co‑cultured CM enhanced pancreatic cancer cell migration and invasion. Mechanistically, SC‑derived Interleukin 6 (IL6), which was induced by co-culture with pancreatic cancer cells, augmented cancer cell migration and invasion by activating STAT3 signaling in cancer cells, while IL6 neutralization or STAT3 downregulation abrogated these effects. Furthermore, Interleukin 1β (IL1β), secreted by tumor cells, activated the nuclear actor (NF)-kappa B pathway in SCs, resulting in increased cytokines production, including IL6, while inhibiting the IL1β-IL1R1 axis led to inactivation of NF-kappa B signaling and downregulated cytokines expression in SCs. Interfering with tumor-neuroglia crosstalk impeded cancer cell dissemination
.
: Schwann cells were extensively distributed in the PDAC tumor microenvironment and high level of intra-tumoral SC markers could serve as an independent prognostic factor for poor survival |
| doi_str_mv | 10.7150/thno.42440 |
| format | Article |
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: Immunofluorescence analysis was performed to reveal the distribution of SCs in PDAC tissues and to determine the prognostic value and clinicopathological relevance of the level of intra‑tumoral SC markers for patients diagnosed with PDAC. Transwell assays and wound healing assays were carried out to investigate the influence of SC conditioned medium (SCM), SC co‑culture, or co-cultured CM on the migratory and invasive abilities of pancreatic cancer cells. The mechanism of SCs induced cancer cells migration and invasion was confirmed using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assays (ELISAs), western blotting, immunofluorescence, immunohistochemistry, siRNA-mediated gene interference, and an
mouse model.
: Immunofluorescence analysis of tissue samples revealed that there were two different types of SCs distributed in the tumor microenvironment, the presence of which correlated with several clinicopathological characteristics and overall survival for patients with PDAC. Although SCM had no impact on the motility and invasiveness of tumor cells, both co-cultivation with SCs and co‑cultured CM enhanced pancreatic cancer cell migration and invasion. Mechanistically, SC‑derived Interleukin 6 (IL6), which was induced by co-culture with pancreatic cancer cells, augmented cancer cell migration and invasion by activating STAT3 signaling in cancer cells, while IL6 neutralization or STAT3 downregulation abrogated these effects. Furthermore, Interleukin 1β (IL1β), secreted by tumor cells, activated the nuclear actor (NF)-kappa B pathway in SCs, resulting in increased cytokines production, including IL6, while inhibiting the IL1β-IL1R1 axis led to inactivation of NF-kappa B signaling and downregulated cytokines expression in SCs. Interfering with tumor-neuroglia crosstalk impeded cancer cell dissemination
.
: Schwann cells were extensively distributed in the PDAC tumor microenvironment and high level of intra-tumoral SC markers could serve as an independent prognostic factor for poor survival of patients with PDAC. The tumor-neuroglia interaction is indispensable for SCs to acquire a tumor-facilitating phenotype. Targeting the tumor-neuroglia interplay might be a promising strategy to treat PDAC.</description><identifier>ISSN: 1838-7640</identifier><identifier>EISSN: 1838-7640</identifier><identifier>DOI: 10.7150/thno.42440</identifier><identifier>PMID: 32308766</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Animals ; Biomarkers, Tumor - metabolism ; Cancer therapies ; Carcinoma, Pancreatic Ductal - immunology ; Carcinoma, Pancreatic Ductal - metabolism ; Carcinoma, Pancreatic Ductal - pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cytokines ; Female ; Glial Fibrillary Acidic Protein - metabolism ; Heterografts ; Humans ; Interleukin-6 - metabolism ; Kinases ; Lung cancer ; Male ; Metastasis ; Mice, SCID ; Middle Aged ; Neoplasm Metastasis ; Neoplasm Staging ; Neuroglia - metabolism ; Neuroglia - pathology ; NF-kappa B p50 Subunit - metabolism ; Pancreatic cancer ; Pancreatic Neoplasms - immunology ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Paracrine Communication ; Reagents ; Research Paper ; Schwann Cells - metabolism ; Schwann Cells - pathology ; STAT3 Transcription Factor - metabolism ; Survival Rate ; Thermal cycling ; Tumor Microenvironment - immunology</subject><ispartof>Theranostics, 2020-01, Vol.10 (11), p.5029-5047</ispartof><rights>The author(s).</rights><rights>2020. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-c483d234df7d09c3435a4360b5cf236a3930e36048b4a39e5248c51491f4cfa63</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7163446/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7163446/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32308766$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Su, Dan</creatorcontrib><creatorcontrib>Guo, Xiaofeng</creatorcontrib><creatorcontrib>Huang, Leyi</creatorcontrib><creatorcontrib>Ye, Huilin</creatorcontrib><creatorcontrib>Li, Zhiguo</creatorcontrib><creatorcontrib>Lin, Longfa</creatorcontrib><creatorcontrib>Chen, Rufu</creatorcontrib><creatorcontrib>Zhou, Quanbo</creatorcontrib><title>Tumor-neuroglia interaction promotes pancreatic cancer metastasis</title><title>Theranostics</title><addtitle>Theranostics</addtitle><description>: The peripheral nervous system (PNS) plays an important role in tumor growth and progression. Schwann cells (SCs), the main glia cells of the PNS, augment cancer metastasis in contact-dependent or contact-independent manner in various malignancies. In the present study, we aimed to determine whether interplay between pancreatic cancer cells and SCs via paracrine signaling contributes to cancer progression.
: Immunofluorescence analysis was performed to reveal the distribution of SCs in PDAC tissues and to determine the prognostic value and clinicopathological relevance of the level of intra‑tumoral SC markers for patients diagnosed with PDAC. Transwell assays and wound healing assays were carried out to investigate the influence of SC conditioned medium (SCM), SC co‑culture, or co-cultured CM on the migratory and invasive abilities of pancreatic cancer cells. The mechanism of SCs induced cancer cells migration and invasion was confirmed using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assays (ELISAs), western blotting, immunofluorescence, immunohistochemistry, siRNA-mediated gene interference, and an
mouse model.
: Immunofluorescence analysis of tissue samples revealed that there were two different types of SCs distributed in the tumor microenvironment, the presence of which correlated with several clinicopathological characteristics and overall survival for patients with PDAC. Although SCM had no impact on the motility and invasiveness of tumor cells, both co-cultivation with SCs and co‑cultured CM enhanced pancreatic cancer cell migration and invasion. Mechanistically, SC‑derived Interleukin 6 (IL6), which was induced by co-culture with pancreatic cancer cells, augmented cancer cell migration and invasion by activating STAT3 signaling in cancer cells, while IL6 neutralization or STAT3 downregulation abrogated these effects. Furthermore, Interleukin 1β (IL1β), secreted by tumor cells, activated the nuclear actor (NF)-kappa B pathway in SCs, resulting in increased cytokines production, including IL6, while inhibiting the IL1β-IL1R1 axis led to inactivation of NF-kappa B signaling and downregulated cytokines expression in SCs. Interfering with tumor-neuroglia crosstalk impeded cancer cell dissemination
.
: Schwann cells were extensively distributed in the PDAC tumor microenvironment and high level of intra-tumoral SC markers could serve as an independent prognostic factor for poor survival of patients with PDAC. The tumor-neuroglia interaction is indispensable for SCs to acquire a tumor-facilitating phenotype. Targeting the tumor-neuroglia interplay might be a promising strategy to treat PDAC.</description><subject>Animals</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cancer therapies</subject><subject>Carcinoma, Pancreatic Ductal - immunology</subject><subject>Carcinoma, Pancreatic Ductal - metabolism</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cytokines</subject><subject>Female</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Heterografts</subject><subject>Humans</subject><subject>Interleukin-6 - metabolism</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Male</subject><subject>Metastasis</subject><subject>Mice, SCID</subject><subject>Middle Aged</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasm Staging</subject><subject>Neuroglia - metabolism</subject><subject>Neuroglia - pathology</subject><subject>NF-kappa B p50 Subunit - metabolism</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - immunology</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Paracrine Communication</subject><subject>Reagents</subject><subject>Research Paper</subject><subject>Schwann Cells - metabolism</subject><subject>Schwann Cells - pathology</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Survival Rate</subject><subject>Thermal cycling</subject><subject>Tumor Microenvironment - immunology</subject><issn>1838-7640</issn><issn>1838-7640</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkU1LxDAQhoMoKqsXf4AUvIhQzce0TS-CLH7Bghc9h2ya7kbapCap4L83u6vL6jBMZpiHlwkvQmcEX1ekwDdxad01UAC8h44JZzyvSsD7O_0ROg3hHacATGtSH6IjRhnmVVkeo7vXsXc-t3r0btEZmRkbtZcqGmezwbveRR2yQVrltYxGZSq12me9jjKkNOEEHbSyC_r0552gt4f71-lTPnt5fJ7ezXIFuIypctZQBk1bNbhWDFghgZV4XqiWslKymmGdZuBzSIMuKHBVEKhJC6qVJZug243uMM573Shto5edGLzppf8SThrxd2PNUizcp6hIyQBWApc_At59jDpE0ZugdNdJq90YBGU1hQrzNXrxD313o7fpe4IWNacFJpwm6mpDKe9C8LrdHkOwWJkjVuaItTkJPt89f4v-WsG-ARANisY</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Su, Dan</creator><creator>Guo, Xiaofeng</creator><creator>Huang, Leyi</creator><creator>Ye, Huilin</creator><creator>Li, Zhiguo</creator><creator>Lin, Longfa</creator><creator>Chen, Rufu</creator><creator>Zhou, Quanbo</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200101</creationdate><title>Tumor-neuroglia interaction promotes pancreatic cancer metastasis</title><author>Su, Dan ; Guo, Xiaofeng ; Huang, Leyi ; Ye, Huilin ; Li, Zhiguo ; Lin, Longfa ; Chen, Rufu ; Zhou, Quanbo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-c483d234df7d09c3435a4360b5cf236a3930e36048b4a39e5248c51491f4cfa63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Cancer therapies</topic><topic>Carcinoma, Pancreatic Ductal - immunology</topic><topic>Carcinoma, Pancreatic Ductal - metabolism</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cytokines</topic><topic>Female</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Heterografts</topic><topic>Humans</topic><topic>Interleukin-6 - metabolism</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Male</topic><topic>Metastasis</topic><topic>Mice, SCID</topic><topic>Middle Aged</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasm Staging</topic><topic>Neuroglia - metabolism</topic><topic>Neuroglia - pathology</topic><topic>NF-kappa B p50 Subunit - metabolism</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - immunology</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Paracrine Communication</topic><topic>Reagents</topic><topic>Research Paper</topic><topic>Schwann Cells - metabolism</topic><topic>Schwann Cells - pathology</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Survival Rate</topic><topic>Thermal cycling</topic><topic>Tumor Microenvironment - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Su, Dan</creatorcontrib><creatorcontrib>Guo, Xiaofeng</creatorcontrib><creatorcontrib>Huang, Leyi</creatorcontrib><creatorcontrib>Ye, Huilin</creatorcontrib><creatorcontrib>Li, Zhiguo</creatorcontrib><creatorcontrib>Lin, Longfa</creatorcontrib><creatorcontrib>Chen, Rufu</creatorcontrib><creatorcontrib>Zhou, Quanbo</creatorcontrib><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>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 Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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 China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Theranostics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Su, Dan</au><au>Guo, Xiaofeng</au><au>Huang, Leyi</au><au>Ye, Huilin</au><au>Li, Zhiguo</au><au>Lin, Longfa</au><au>Chen, Rufu</au><au>Zhou, Quanbo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor-neuroglia interaction promotes pancreatic cancer metastasis</atitle><jtitle>Theranostics</jtitle><addtitle>Theranostics</addtitle><date>2020-01-01</date><risdate>2020</risdate><volume>10</volume><issue>11</issue><spage>5029</spage><epage>5047</epage><pages>5029-5047</pages><issn>1838-7640</issn><eissn>1838-7640</eissn><abstract>: The peripheral nervous system (PNS) plays an important role in tumor growth and progression. Schwann cells (SCs), the main glia cells of the PNS, augment cancer metastasis in contact-dependent or contact-independent manner in various malignancies. In the present study, we aimed to determine whether interplay between pancreatic cancer cells and SCs via paracrine signaling contributes to cancer progression.
: Immunofluorescence analysis was performed to reveal the distribution of SCs in PDAC tissues and to determine the prognostic value and clinicopathological relevance of the level of intra‑tumoral SC markers for patients diagnosed with PDAC. Transwell assays and wound healing assays were carried out to investigate the influence of SC conditioned medium (SCM), SC co‑culture, or co-cultured CM on the migratory and invasive abilities of pancreatic cancer cells. The mechanism of SCs induced cancer cells migration and invasion was confirmed using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assays (ELISAs), western blotting, immunofluorescence, immunohistochemistry, siRNA-mediated gene interference, and an
mouse model.
: Immunofluorescence analysis of tissue samples revealed that there were two different types of SCs distributed in the tumor microenvironment, the presence of which correlated with several clinicopathological characteristics and overall survival for patients with PDAC. Although SCM had no impact on the motility and invasiveness of tumor cells, both co-cultivation with SCs and co‑cultured CM enhanced pancreatic cancer cell migration and invasion. Mechanistically, SC‑derived Interleukin 6 (IL6), which was induced by co-culture with pancreatic cancer cells, augmented cancer cell migration and invasion by activating STAT3 signaling in cancer cells, while IL6 neutralization or STAT3 downregulation abrogated these effects. Furthermore, Interleukin 1β (IL1β), secreted by tumor cells, activated the nuclear actor (NF)-kappa B pathway in SCs, resulting in increased cytokines production, including IL6, while inhibiting the IL1β-IL1R1 axis led to inactivation of NF-kappa B signaling and downregulated cytokines expression in SCs. Interfering with tumor-neuroglia crosstalk impeded cancer cell dissemination
.
: Schwann cells were extensively distributed in the PDAC tumor microenvironment and high level of intra-tumoral SC markers could serve as an independent prognostic factor for poor survival of patients with PDAC. The tumor-neuroglia interaction is indispensable for SCs to acquire a tumor-facilitating phenotype. Targeting the tumor-neuroglia interplay might be a promising strategy to treat PDAC.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>32308766</pmid><doi>10.7150/thno.42440</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Theranostics, 2020-01, Vol.10 (11), p.5029-5047 |
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| subjects | Animals Biomarkers, Tumor - metabolism Cancer therapies Carcinoma, Pancreatic Ductal - immunology Carcinoma, Pancreatic Ductal - metabolism Carcinoma, Pancreatic Ductal - pathology Cell Line, Tumor Cell Movement Cell Proliferation Cytokines Female Glial Fibrillary Acidic Protein - metabolism Heterografts Humans Interleukin-6 - metabolism Kinases Lung cancer Male Metastasis Mice, SCID Middle Aged Neoplasm Metastasis Neoplasm Staging Neuroglia - metabolism Neuroglia - pathology NF-kappa B p50 Subunit - metabolism Pancreatic cancer Pancreatic Neoplasms - immunology Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Paracrine Communication Reagents Research Paper Schwann Cells - metabolism Schwann Cells - pathology STAT3 Transcription Factor - metabolism Survival Rate Thermal cycling Tumor Microenvironment - immunology |
| title | Tumor-neuroglia interaction promotes pancreatic cancer metastasis |
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