IL-39 acts as a friend to pancreatic cancer
Pancreatic cancer is the most lethal digestive cancer and the fourth leading cause of cancer death in the US. IL-39, a heterodimer of p19 and EBI3, is a newly found cytokine and its role in the pathogenesis of neoplasia has not been studied yet. This study was designed to investigate the direct role...
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| Veröffentlicht in: | Medical oncology (Northwood, London, England) London, England), 2019, Vol.36 (1), p.12-7, Article 12 |
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| creator | Manning, Alicia A. Zhao, Lei Zhu, Ziwen Xiao, Huaping Redington, Chase G. Ding, Vivi A. Stewart-Hester, Theodore Bai, Qian Dunlap, Jacob Wakefield, Mark R. Fang, Yujiang |
| description | Pancreatic cancer is the most lethal digestive cancer and the fourth leading cause of cancer death in the US. IL-39, a heterodimer of p19 and EBI3, is a newly found cytokine and its role in the pathogenesis of neoplasia has not been studied yet. This study was designed to investigate the direct role of IL-39 in the growth of pancreatic cancer. Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the direct effects of IL-39 on cell survival, proliferation and apoptosis of the widely studied pancreatic cancer cell line MiaPaCa-2. We further investigated the possible molecular mechanisms by using RT-PCR and IHC. The percentage of colonies of pancreatic cancer cells increased significantly in the presence of IL-39. This was paralleled with the increase in the OD value of cancer cells in the presence of IL-39. Interestingly, the relative caspase-3 activity in cancer cells decreased significantly in the presence of IL-39. Furthermore, the pro-tumor effect of IL-39 on pancreatic cancer cells correlated with decreased anti-proliferative molecule p21.The anti-apoptotic effect of IL-39 correlated with decreased pro-apoptotic molecule TRAILR1. These results suggest that IL-39 favors growth of pancreatic cancer by promoting growth and inhibiting apoptosis of cancer cells. This suggests that IL-39 acts as a friend to pancreatic cancer. Thus, inhibition of effect of IL-39 on cells might be a promising strategy to treat pancreatic cancer. |
| doi_str_mv | 10.1007/s12032-018-1236-y |
| format | Article |
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IL-39, a heterodimer of p19 and EBI3, is a newly found cytokine and its role in the pathogenesis of neoplasia has not been studied yet. This study was designed to investigate the direct role of IL-39 in the growth of pancreatic cancer. Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the direct effects of IL-39 on cell survival, proliferation and apoptosis of the widely studied pancreatic cancer cell line MiaPaCa-2. We further investigated the possible molecular mechanisms by using RT-PCR and IHC. The percentage of colonies of pancreatic cancer cells increased significantly in the presence of IL-39. This was paralleled with the increase in the OD value of cancer cells in the presence of IL-39. Interestingly, the relative caspase-3 activity in cancer cells decreased significantly in the presence of IL-39. Furthermore, the pro-tumor effect of IL-39 on pancreatic cancer cells correlated with decreased anti-proliferative molecule p21.The anti-apoptotic effect of IL-39 correlated with decreased pro-apoptotic molecule TRAILR1. These results suggest that IL-39 favors growth of pancreatic cancer by promoting growth and inhibiting apoptosis of cancer cells. This suggests that IL-39 acts as a friend to pancreatic cancer. Thus, inhibition of effect of IL-39 on cells might be a promising strategy to treat pancreatic cancer.</description><identifier>ISSN: 1357-0560</identifier><identifier>ISSN: 1559-131X</identifier><identifier>EISSN: 1559-131X</identifier><identifier>DOI: 10.1007/s12032-018-1236-y</identifier><identifier>PMID: 30506430</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>APOPTOSIS ; Apoptosis - physiology ; Cell Growth Processes - physiology ; Cell Line, Tumor ; CELL PROLIFERATION ; Hematology ; Humans ; Immunohistochemistry ; Interleukins - biosynthesis ; Internal Medicine ; LYMPHOKINES ; Medicine ; Medicine & Public Health ; NEOPLASMS ; Oncology ; Original Paper ; PANCREAS ; Pancreatic cancer ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; PATHOGENESIS ; Pathology ; POLYMERASE CHAIN REACTION ; RADIOLOGY AND NUCLEAR MEDICINE ; Reverse Transcriptase Polymerase Chain Reaction</subject><ispartof>Medical oncology (Northwood, London, England), 2019, Vol.36 (1), p.12-7, Article 12</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2018</rights><rights>Medical Oncology is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c315y-cd17946e26aa54125d07d06f02b26824a4af1e606a0aa08242bc30797c7fb29e3</citedby><cites>FETCH-LOGICAL-c315y-cd17946e26aa54125d07d06f02b26824a4af1e606a0aa08242bc30797c7fb29e3</cites><orcidid>0000-0002-9107-7374</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12032-018-1236-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12032-018-1236-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30506430$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22938452$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Manning, Alicia A.</creatorcontrib><creatorcontrib>Zhao, Lei</creatorcontrib><creatorcontrib>Zhu, Ziwen</creatorcontrib><creatorcontrib>Xiao, Huaping</creatorcontrib><creatorcontrib>Redington, Chase G.</creatorcontrib><creatorcontrib>Ding, Vivi A.</creatorcontrib><creatorcontrib>Stewart-Hester, Theodore</creatorcontrib><creatorcontrib>Bai, Qian</creatorcontrib><creatorcontrib>Dunlap, Jacob</creatorcontrib><creatorcontrib>Wakefield, Mark R.</creatorcontrib><creatorcontrib>Fang, Yujiang</creatorcontrib><title>IL-39 acts as a friend to pancreatic cancer</title><title>Medical oncology (Northwood, London, England)</title><addtitle>Med Oncol</addtitle><addtitle>Med Oncol</addtitle><description>Pancreatic cancer is the most lethal digestive cancer and the fourth leading cause of cancer death in the US. IL-39, a heterodimer of p19 and EBI3, is a newly found cytokine and its role in the pathogenesis of neoplasia has not been studied yet. This study was designed to investigate the direct role of IL-39 in the growth of pancreatic cancer. Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the direct effects of IL-39 on cell survival, proliferation and apoptosis of the widely studied pancreatic cancer cell line MiaPaCa-2. We further investigated the possible molecular mechanisms by using RT-PCR and IHC. The percentage of colonies of pancreatic cancer cells increased significantly in the presence of IL-39. This was paralleled with the increase in the OD value of cancer cells in the presence of IL-39. Interestingly, the relative caspase-3 activity in cancer cells decreased significantly in the presence of IL-39. Furthermore, the pro-tumor effect of IL-39 on pancreatic cancer cells correlated with decreased anti-proliferative molecule p21.The anti-apoptotic effect of IL-39 correlated with decreased pro-apoptotic molecule TRAILR1. These results suggest that IL-39 favors growth of pancreatic cancer by promoting growth and inhibiting apoptosis of cancer cells. This suggests that IL-39 acts as a friend to pancreatic cancer. Thus, inhibition of effect of IL-39 on cells might be a promising strategy to treat pancreatic cancer.</description><subject>APOPTOSIS</subject><subject>Apoptosis - physiology</subject><subject>Cell Growth Processes - physiology</subject><subject>Cell Line, Tumor</subject><subject>CELL PROLIFERATION</subject><subject>Hematology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Interleukins - biosynthesis</subject><subject>Internal Medicine</subject><subject>LYMPHOKINES</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>NEOPLASMS</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>PANCREAS</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>PATHOGENESIS</subject><subject>Pathology</subject><subject>POLYMERASE CHAIN REACTION</subject><subject>RADIOLOGY AND NUCLEAR MEDICINE</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><issn>1357-0560</issn><issn>1559-131X</issn><issn>1559-131X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kE1LAzEQhoMoVqs_wIsseBEkOpl87R6l-FEoeFHwFtJsVre0uzXZPfTfm7K1PQkhGZJn3iEPIVcM7hmAfogMgSMFllOGXNHNETljUhaUcfZ5nGouNQWpYETOY1wAIJNYnJIRBwlKcDgjd9MZ5UVmXRczm1ZWhdo3Zda12do2Lnjb1S5zqfThgpxUdhn95e4ck4_np_fJK529vUwnjzPqOJMb6kqmC6E8KmulYChL0CWoCnCOKkdhha2YV6AsWAvpAueOgy6009UcC8_H5GbIbWNXm-jqzrtv1zaNd51BLHguJCbqdqDWof3pfezMqo7OL5e28W0fDTJRAEKu5SFwjy7aPjTpD1sKhNBpSxQbKBfaGIOvzDrUKxs2hoHZ-jaDb5N8m61vs0k917vkfr7y5b7jT3ACcABiemq-fDiM_j_1FxaNhk8</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Manning, Alicia A.</creator><creator>Zhao, Lei</creator><creator>Zhu, Ziwen</creator><creator>Xiao, Huaping</creator><creator>Redington, Chase G.</creator><creator>Ding, Vivi A.</creator><creator>Stewart-Hester, Theodore</creator><creator>Bai, Qian</creator><creator>Dunlap, Jacob</creator><creator>Wakefield, Mark R.</creator><creator>Fang, Yujiang</creator><general>Springer US</general><general>Springer Nature B.V</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>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>OTOTI</scope><orcidid>https://orcid.org/0000-0002-9107-7374</orcidid></search><sort><creationdate>2019</creationdate><title>IL-39 acts as a friend to pancreatic cancer</title><author>Manning, Alicia A. ; 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IL-39, a heterodimer of p19 and EBI3, is a newly found cytokine and its role in the pathogenesis of neoplasia has not been studied yet. This study was designed to investigate the direct role of IL-39 in the growth of pancreatic cancer. Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the direct effects of IL-39 on cell survival, proliferation and apoptosis of the widely studied pancreatic cancer cell line MiaPaCa-2. We further investigated the possible molecular mechanisms by using RT-PCR and IHC. The percentage of colonies of pancreatic cancer cells increased significantly in the presence of IL-39. This was paralleled with the increase in the OD value of cancer cells in the presence of IL-39. Interestingly, the relative caspase-3 activity in cancer cells decreased significantly in the presence of IL-39. Furthermore, the pro-tumor effect of IL-39 on pancreatic cancer cells correlated with decreased anti-proliferative molecule p21.The anti-apoptotic effect of IL-39 correlated with decreased pro-apoptotic molecule TRAILR1. These results suggest that IL-39 favors growth of pancreatic cancer by promoting growth and inhibiting apoptosis of cancer cells. This suggests that IL-39 acts as a friend to pancreatic cancer. Thus, inhibition of effect of IL-39 on cells might be a promising strategy to treat pancreatic cancer.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30506430</pmid><doi>10.1007/s12032-018-1236-y</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-9107-7374</orcidid></addata></record> |
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| ispartof | Medical oncology (Northwood, London, England), 2019, Vol.36 (1), p.12-7, Article 12 |
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| subjects | APOPTOSIS Apoptosis - physiology Cell Growth Processes - physiology Cell Line, Tumor CELL PROLIFERATION Hematology Humans Immunohistochemistry Interleukins - biosynthesis Internal Medicine LYMPHOKINES Medicine Medicine & Public Health NEOPLASMS Oncology Original Paper PANCREAS Pancreatic cancer Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology PATHOGENESIS Pathology POLYMERASE CHAIN REACTION RADIOLOGY AND NUCLEAR MEDICINE Reverse Transcriptase Polymerase Chain Reaction |
| title | IL-39 acts as a friend to pancreatic cancer |
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