GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway
Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor that is characterized by its high proliferative and migratory potential, leading to a high invasiveness of this tumor type. However, the underlying mechanism of GBM proliferation and migration has not been fully elucidate...
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description | Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor that is characterized by its high proliferative and migratory potential, leading to a high invasiveness of this tumor type. However, the underlying mechanism of GBM proliferation and migration has not been fully elucidated. In this study, at first, we used RNA-seq together with bioinformatics technology to screen for C-X-C motif ligand 1 (CXCL1) as a proliferation-related gene. And exogenous glial cell line-derived neurotrophic factor (GDNF) induced proliferation and up-regulated the level of CXCL1 in rat C6 glioma cells determined by sqPCR and ELISA. Then, we manipulated the CXCL1 expression by using a lentiviral vector (CXCL1-RNAi) approach. By this, the proliferation of C6 cells was decreased, suggesting that CXCL1 plays a key role in proliferation in these cells. We hypothesized that exogenous GDNF promoted NF-κB nuclear translocation and therefore, analyzed the interaction of CXCL1 with NF-κB by Western Blot and immunofluorescence. Additionally, we used BAY 11–7082, a phosphorylation inhibitor of NF-κB, to elucidate NF-κB mediated the effect of GDNF on CXCL1. These results demonstrated that GDNF enhanced the proliferation of rat C6 glioma cells through activating the NF-κB/CXCL1 signaling pathway. In summary, these studies not only revealed the mechanism of action of exogenous GDNF in promoting the proliferation of C6 glioma cells but may also provide a new biological target for the treatment of malignant glioma. |
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However, the underlying mechanism of GBM proliferation and migration has not been fully elucidated. In this study, at first, we used RNA-seq together with bioinformatics technology to screen for C-X-C motif ligand 1 (CXCL1) as a proliferation-related gene. And exogenous glial cell line-derived neurotrophic factor (GDNF) induced proliferation and up-regulated the level of CXCL1 in rat C6 glioma cells determined by sqPCR and ELISA. Then, we manipulated the CXCL1 expression by using a lentiviral vector (CXCL1-RNAi) approach. By this, the proliferation of C6 cells was decreased, suggesting that CXCL1 plays a key role in proliferation in these cells. We hypothesized that exogenous GDNF promoted NF-κB nuclear translocation and therefore, analyzed the interaction of CXCL1 with NF-κB by Western Blot and immunofluorescence. Additionally, we used BAY 11–7082, a phosphorylation inhibitor of NF-κB, to elucidate NF-κB mediated the effect of GDNF on CXCL1. These results demonstrated that GDNF enhanced the proliferation of rat C6 glioma cells through activating the NF-κB/CXCL1 signaling pathway. In summary, these studies not only revealed the mechanism of action of exogenous GDNF in promoting the proliferation of C6 glioma cells but may also provide a new biological target for the treatment of malignant glioma.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0289071</identifier><identifier>PMID: 37594930</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Bioinformatics ; Biology and Life Sciences ; Brain cancer ; Brain tumors ; Cell proliferation ; Enzyme-linked immunosorbent assay ; Gene expression ; Glial cell line-derived neurotrophic factor ; Glial cells ; Glioblastoma ; Glioma ; Glioma cells ; Immunofluorescence ; Invasiveness ; Medicine and Health Sciences ; Neuronal-glial interactions ; Neurotrophic factors ; NF-κB protein ; Nuclear transport ; Phosphorylation ; Proteins ; Research and Analysis Methods ; RNA-mediated interference ; Signal transduction ; Software ; Survival analysis ; Translocation ; Tumors</subject><ispartof>PloS one, 2023-08, Vol.18 (8), p.e0289071-e0289071</ispartof><rights>2023 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 Wang et al 2023 Wang et al</rights><rights>2023 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c387t-64affe661c9ef23a26477575acc6d265b5a0a6f4d1fd1b7255df11232910e6923</cites><orcidid>0000-0001-8567-0238 ; 0000-0002-5938-4243</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10437914/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10437914/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids></links><search><creatorcontrib>Wang, Yue</creatorcontrib><creatorcontrib>Wu, Yue</creatorcontrib><creatorcontrib>Li, Li</creatorcontrib><creatorcontrib>Gao, Jin</creatorcontrib><creatorcontrib>Gao, Dian Shuai</creatorcontrib><creatorcontrib>Sun, Shen</creatorcontrib><title>GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway</title><title>PloS one</title><description>Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor that is characterized by its high proliferative and migratory potential, leading to a high invasiveness of this tumor type. However, the underlying mechanism of GBM proliferation and migration has not been fully elucidated. In this study, at first, we used RNA-seq together with bioinformatics technology to screen for C-X-C motif ligand 1 (CXCL1) as a proliferation-related gene. And exogenous glial cell line-derived neurotrophic factor (GDNF) induced proliferation and up-regulated the level of CXCL1 in rat C6 glioma cells determined by sqPCR and ELISA. Then, we manipulated the CXCL1 expression by using a lentiviral vector (CXCL1-RNAi) approach. By this, the proliferation of C6 cells was decreased, suggesting that CXCL1 plays a key role in proliferation in these cells. We hypothesized that exogenous GDNF promoted NF-κB nuclear translocation and therefore, analyzed the interaction of CXCL1 with NF-κB by Western Blot and immunofluorescence. Additionally, we used BAY 11–7082, a phosphorylation inhibitor of NF-κB, to elucidate NF-κB mediated the effect of GDNF on CXCL1. These results demonstrated that GDNF enhanced the proliferation of rat C6 glioma cells through activating the NF-κB/CXCL1 signaling pathway. In summary, these studies not only revealed the mechanism of action of exogenous GDNF in promoting the proliferation of C6 glioma cells but may also provide a new biological target for the treatment of malignant glioma.</description><subject>Bioinformatics</subject><subject>Biology and Life Sciences</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Cell proliferation</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gene expression</subject><subject>Glial cell line-derived neurotrophic factor</subject><subject>Glial cells</subject><subject>Glioblastoma</subject><subject>Glioma</subject><subject>Glioma cells</subject><subject>Immunofluorescence</subject><subject>Invasiveness</subject><subject>Medicine and Health Sciences</subject><subject>Neuronal-glial interactions</subject><subject>Neurotrophic factors</subject><subject>NF-κB protein</subject><subject>Nuclear 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triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway</title><author>Wang, Yue ; Wu, Yue ; Li, Li ; Gao, Jin ; Gao, Dian Shuai ; Sun, Shen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-64affe661c9ef23a26477575acc6d265b5a0a6f4d1fd1b7255df11232910e6923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Bioinformatics</topic><topic>Biology and Life Sciences</topic><topic>Brain cancer</topic><topic>Brain tumors</topic><topic>Cell proliferation</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gene expression</topic><topic>Glial cell line-derived neurotrophic factor</topic><topic>Glial cells</topic><topic>Glioblastoma</topic><topic>Glioma</topic><topic>Glioma cells</topic><topic>Immunofluorescence</topic><topic>Invasiveness</topic><topic>Medicine and Health Sciences</topic><topic>Neuronal-glial 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Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yue</au><au>Wu, Yue</au><au>Li, Li</au><au>Gao, Jin</au><au>Gao, Dian Shuai</au><au>Sun, Shen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway</atitle><jtitle>PloS one</jtitle><date>2023-08-18</date><risdate>2023</risdate><volume>18</volume><issue>8</issue><spage>e0289071</spage><epage>e0289071</epage><pages>e0289071-e0289071</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor that is characterized by its high proliferative and migratory potential, leading to a high invasiveness of this tumor type. However, the underlying mechanism of GBM proliferation and migration has not been fully elucidated. In this study, at first, we used RNA-seq together with bioinformatics technology to screen for C-X-C motif ligand 1 (CXCL1) as a proliferation-related gene. And exogenous glial cell line-derived neurotrophic factor (GDNF) induced proliferation and up-regulated the level of CXCL1 in rat C6 glioma cells determined by sqPCR and ELISA. Then, we manipulated the CXCL1 expression by using a lentiviral vector (CXCL1-RNAi) approach. By this, the proliferation of C6 cells was decreased, suggesting that CXCL1 plays a key role in proliferation in these cells. We hypothesized that exogenous GDNF promoted NF-κB nuclear translocation and therefore, analyzed the interaction of CXCL1 with NF-κB by Western Blot and immunofluorescence. Additionally, we used BAY 11–7082, a phosphorylation inhibitor of NF-κB, to elucidate NF-κB mediated the effect of GDNF on CXCL1. These results demonstrated that GDNF enhanced the proliferation of rat C6 glioma cells through activating the NF-κB/CXCL1 signaling pathway. In summary, these studies not only revealed the mechanism of action of exogenous GDNF in promoting the proliferation of C6 glioma cells but may also provide a new biological target for the treatment of malignant glioma.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>37594930</pmid><doi>10.1371/journal.pone.0289071</doi><orcidid>https://orcid.org/0000-0001-8567-0238</orcidid><orcidid>https://orcid.org/0000-0002-5938-4243</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Bioinformatics Biology and Life Sciences Brain cancer Brain tumors Cell proliferation Enzyme-linked immunosorbent assay Gene expression Glial cell line-derived neurotrophic factor Glial cells Glioblastoma Glioma Glioma cells Immunofluorescence Invasiveness Medicine and Health Sciences Neuronal-glial interactions Neurotrophic factors NF-κB protein Nuclear transport Phosphorylation Proteins Research and Analysis Methods RNA-mediated interference Signal transduction Software Survival analysis Translocation Tumors |
title | GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway |
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