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Activation of PTGS2/NF‐κB signaling pathway enhances radiation resistance of glioma

OBJECTIVE: We focused on the effects of PTGS2/NF‐κB signaling pathway on the radiation resistance of glioma in the study. METHODS: We downloaded the microarray data from the Gene Expression Omnibus (GEO) database. We verified transfection successfully through QRT‐PCR analysis. Immunofluorescence was...

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Detalles Bibliográficos
Autores principales: Tan, Cheng, Liu, Liang, Liu, Xiaoyang, Qi, Ling, Wang, Weiyao, Zhao, Guifang, Wang, Libo, Dai, Yimeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6434213/
https://www.ncbi.nlm.nih.gov/pubmed/30740906
http://dx.doi.org/10.1002/cam4.1971
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author Tan, Cheng
Liu, Liang
Liu, Xiaoyang
Qi, Ling
Wang, Weiyao
Zhao, Guifang
Wang, Libo
Dai, Yimeng
author_facet Tan, Cheng
Liu, Liang
Liu, Xiaoyang
Qi, Ling
Wang, Weiyao
Zhao, Guifang
Wang, Libo
Dai, Yimeng
author_sort Tan, Cheng
collection PubMed
description OBJECTIVE: We focused on the effects of PTGS2/NF‐κB signaling pathway on the radiation resistance of glioma in the study. METHODS: We downloaded the microarray data from the Gene Expression Omnibus (GEO) database. We verified transfection successfully through QRT‐PCR analysis. Immunofluorescence was used to detect γH2AX content under 2 Gy radiation. The survival rates of cells under 2 Gy irradiation were tested by clonogenic survival assay. Flow cytometry was used to detect cell cycle. Western blot was applied to detect the expression of NF‐κB pathway‐related proteins. We also used MTT assay to detect the proliferation of cells. RESULTS: In this research, we discovered that the expression of the PTGS2 was upregulated in radiation‐resistant glioma cells. The radio‐tolerance rate of U87 cells was obviously elevated after the overexpression of PTGS2. The radioresistance of U87R cells was significantly reduced after the knockdown of PTGS2. After radiotherapy, the number of cells arrested in G2/M phase decreased after PTGS2 overexpression in U87cells but increased in PTGS2 knockdown in U87R cells. The survival rate of U87 and U87R cells under radiation decreased significantly after the addition of NF‐κB inhibitor. The proliferation of U87 cells was suppressed by radiation and the addition of Bay 11. In addition, PTGS2 activated NF‐κB signaling pathway and prevented DNA damage after radiotherapy. Lastly, PTGS2 was proved to facilitate tumor cell proliferation and improve the radio‐tolerance. CONCLUSION: PTGS2/NF‐κB signaling pathway was involved in radio‐tolerance of glioma cells, which provided a new insight into glioma therapy.
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spelling pubmed-64342132019-04-08 Activation of PTGS2/NF‐κB signaling pathway enhances radiation resistance of glioma Tan, Cheng Liu, Liang Liu, Xiaoyang Qi, Ling Wang, Weiyao Zhao, Guifang Wang, Libo Dai, Yimeng Cancer Med Cancer Biology OBJECTIVE: We focused on the effects of PTGS2/NF‐κB signaling pathway on the radiation resistance of glioma in the study. METHODS: We downloaded the microarray data from the Gene Expression Omnibus (GEO) database. We verified transfection successfully through QRT‐PCR analysis. Immunofluorescence was used to detect γH2AX content under 2 Gy radiation. The survival rates of cells under 2 Gy irradiation were tested by clonogenic survival assay. Flow cytometry was used to detect cell cycle. Western blot was applied to detect the expression of NF‐κB pathway‐related proteins. We also used MTT assay to detect the proliferation of cells. RESULTS: In this research, we discovered that the expression of the PTGS2 was upregulated in radiation‐resistant glioma cells. The radio‐tolerance rate of U87 cells was obviously elevated after the overexpression of PTGS2. The radioresistance of U87R cells was significantly reduced after the knockdown of PTGS2. After radiotherapy, the number of cells arrested in G2/M phase decreased after PTGS2 overexpression in U87cells but increased in PTGS2 knockdown in U87R cells. The survival rate of U87 and U87R cells under radiation decreased significantly after the addition of NF‐κB inhibitor. The proliferation of U87 cells was suppressed by radiation and the addition of Bay 11. In addition, PTGS2 activated NF‐κB signaling pathway and prevented DNA damage after radiotherapy. Lastly, PTGS2 was proved to facilitate tumor cell proliferation and improve the radio‐tolerance. CONCLUSION: PTGS2/NF‐κB signaling pathway was involved in radio‐tolerance of glioma cells, which provided a new insight into glioma therapy. John Wiley and Sons Inc. 2019-02-10 /pmc/articles/PMC6434213/ /pubmed/30740906 http://dx.doi.org/10.1002/cam4.1971 Text en © 2019 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Cancer Biology
Tan, Cheng
Liu, Liang
Liu, Xiaoyang
Qi, Ling
Wang, Weiyao
Zhao, Guifang
Wang, Libo
Dai, Yimeng
Activation of PTGS2/NF‐κB signaling pathway enhances radiation resistance of glioma
title Activation of PTGS2/NF‐κB signaling pathway enhances radiation resistance of glioma
title_full Activation of PTGS2/NF‐κB signaling pathway enhances radiation resistance of glioma
title_fullStr Activation of PTGS2/NF‐κB signaling pathway enhances radiation resistance of glioma
title_full_unstemmed Activation of PTGS2/NF‐κB signaling pathway enhances radiation resistance of glioma
title_short Activation of PTGS2/NF‐κB signaling pathway enhances radiation resistance of glioma
title_sort activation of ptgs2/nf‐κb signaling pathway enhances radiation resistance of glioma
topic Cancer Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6434213/
https://www.ncbi.nlm.nih.gov/pubmed/30740906
http://dx.doi.org/10.1002/cam4.1971
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