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Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells

BACKGROUND: Eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) is an important factor regulating protein translation. It also impacts proliferation, apoptosis, invasion, and the cell cycle of cancer cells. The aim of this study was to investigate the relationship between 4E-BP1 a...

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Autores principales: Li, Lei, Zhang, Li, Liu, Dan, Cheng, Yue, Jing, Yu-ting, Yu, He, Zhou, Ping, Song, Juan, Li, Wei-min
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511320/
https://www.ncbi.nlm.nih.gov/pubmed/26273397
http://dx.doi.org/10.1111/1759-7714.12196
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author Li, Lei
Zhang, Li
Liu, Dan
Cheng, Yue
Jing, Yu-ting
Yu, He
Zhou, Ping
Song, Juan
Li, Wei-min
author_facet Li, Lei
Zhang, Li
Liu, Dan
Cheng, Yue
Jing, Yu-ting
Yu, He
Zhou, Ping
Song, Juan
Li, Wei-min
author_sort Li, Lei
collection PubMed
description BACKGROUND: Eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) is an important factor regulating protein translation. It also impacts proliferation, apoptosis, invasion, and the cell cycle of cancer cells. The aim of this study was to investigate the relationship between 4E-BP1 and human immune status, recognizing immunomodulatory molecules involved in the overexpression of 4E-BP1. METHODS: A lentivirus expression system was used to overexpress 4E-BP1 in the H1299 cell line. Western blot was performed to investigate the expression level of 4E-BP1 and P-4E-BP1, and quantitative polymerase chain reaction was used to quantify gene expression of immunomodulatory molecules. RESULTS: The expression level of 4E-BP1 increased significantly after lentivirus infection (P < 0.05). Overexpression of 4E-BP1 upregulated the expression of interleukin (IL)-1β (P < 0.05), IL-5 (P < 0.001), IL-23 (P < 0.001), macrophage inflammatory protein-1β (P < 0.001), Eota-3 (P < 0.05), and MCP-4 (P < 0.05). Most of the increases were observed at the seventh day. The variation trend of IL-10, cell division cycle protein 2, proliferating cell nuclear antigen, and phosphatase and tensin homolog was not clear. CONCLUSION: Overexpression of 4E-BP1 altered immune status by upregulating the expression of a series of immunomodulatory molecules, indicating that 4E-BP1 could serve as a potential therapeutic target against cancer.
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spelling pubmed-45113202015-08-13 Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells Li, Lei Zhang, Li Liu, Dan Cheng, Yue Jing, Yu-ting Yu, He Zhou, Ping Song, Juan Li, Wei-min Thorac Cancer Original Articles BACKGROUND: Eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) is an important factor regulating protein translation. It also impacts proliferation, apoptosis, invasion, and the cell cycle of cancer cells. The aim of this study was to investigate the relationship between 4E-BP1 and human immune status, recognizing immunomodulatory molecules involved in the overexpression of 4E-BP1. METHODS: A lentivirus expression system was used to overexpress 4E-BP1 in the H1299 cell line. Western blot was performed to investigate the expression level of 4E-BP1 and P-4E-BP1, and quantitative polymerase chain reaction was used to quantify gene expression of immunomodulatory molecules. RESULTS: The expression level of 4E-BP1 increased significantly after lentivirus infection (P < 0.05). Overexpression of 4E-BP1 upregulated the expression of interleukin (IL)-1β (P < 0.05), IL-5 (P < 0.001), IL-23 (P < 0.001), macrophage inflammatory protein-1β (P < 0.001), Eota-3 (P < 0.05), and MCP-4 (P < 0.05). Most of the increases were observed at the seventh day. The variation trend of IL-10, cell division cycle protein 2, proliferating cell nuclear antigen, and phosphatase and tensin homolog was not clear. CONCLUSION: Overexpression of 4E-BP1 altered immune status by upregulating the expression of a series of immunomodulatory molecules, indicating that 4E-BP1 could serve as a potential therapeutic target against cancer. John Wiley & Sons, Ltd 2015-07 2015-07-02 /pmc/articles/PMC4511320/ /pubmed/26273397 http://dx.doi.org/10.1111/1759-7714.12196 Text en © 2014 The Authors. Thoracic Cancer published by Tianjin Lung Cancer Institute and Wiley Publishing Asia Pty Ltd. http://creativecommons.org/licenses/by-nc/4.0/ This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Articles
Li, Lei
Zhang, Li
Liu, Dan
Cheng, Yue
Jing, Yu-ting
Yu, He
Zhou, Ping
Song, Juan
Li, Wei-min
Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells
title Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells
title_full Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells
title_fullStr Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells
title_full_unstemmed Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells
title_short Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells
title_sort overexpression of eukaryotic translation initiation factor 4e-binding protein 1 induces the alteration of immune status in h1299 lung cancer cells
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511320/
https://www.ncbi.nlm.nih.gov/pubmed/26273397
http://dx.doi.org/10.1111/1759-7714.12196
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