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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Veröffentlicht in:PloS one 2023-08, Vol.18 (8), p.e0289071-e0289071
Hauptverfasser: Wang, Yue, Wu, Yue, Li, Li, Gao, Jin, Gao, Dian Shuai, Sun, Shen
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Li, Li
Gao, Jin
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Sun, Shen
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. 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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.</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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