Cargando…
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...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2023
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10437914/ https://www.ncbi.nlm.nih.gov/pubmed/37594930 http://dx.doi.org/10.1371/journal.pone.0289071 |
_version_ | 1785092646302121984 |
---|---|
author | Wang, Yue Wu, Yue Li, Li Gao, Jin Gao, Dian Shuai Sun, Shen |
author_facet | Wang, Yue Wu, Yue Li, Li Gao, Jin Gao, Dian Shuai Sun, Shen |
author_sort | Wang, Yue |
collection | PubMed |
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. |
format | Online Article Text |
id | pubmed-10437914 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-104379142023-08-19 GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway Wang, Yue Wu, Yue Li, Li Gao, Jin Gao, Dian Shuai Sun, Shen PLoS One Research Article 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. Public Library of Science 2023-08-18 /pmc/articles/PMC10437914/ /pubmed/37594930 http://dx.doi.org/10.1371/journal.pone.0289071 Text en © 2023 Wang et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Wang, Yue Wu, Yue Li, Li Gao, Jin Gao, Dian Shuai Sun, Shen GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway |
title | GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway |
title_full | GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway |
title_fullStr | GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway |
title_full_unstemmed | GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway |
title_short | GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway |
title_sort | gdnf triggers proliferation of rat c6 glioma cells via the nf-κb/cxcl1 signaling pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10437914/ https://www.ncbi.nlm.nih.gov/pubmed/37594930 http://dx.doi.org/10.1371/journal.pone.0289071 |
work_keys_str_mv | AT wangyue gdnftriggersproliferationofratc6gliomacellsviathenfkbcxcl1signalingpathway AT wuyue gdnftriggersproliferationofratc6gliomacellsviathenfkbcxcl1signalingpathway AT lili gdnftriggersproliferationofratc6gliomacellsviathenfkbcxcl1signalingpathway AT gaojin gdnftriggersproliferationofratc6gliomacellsviathenfkbcxcl1signalingpathway AT gaodianshuai gdnftriggersproliferationofratc6gliomacellsviathenfkbcxcl1signalingpathway AT sunshen gdnftriggersproliferationofratc6gliomacellsviathenfkbcxcl1signalingpathway |