1. Overexpression of eukaryotic translation initiation factor 4E-binding protein 1 induces the alteration of immune status in H1299 lung cancer cells.
- Author
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Li, Lei, Zhang, Li, Liu, Dan, Cheng, Yue, Jing, Yu‐ting, Yu, He, Zhou, Ping, Song, Juan, and Li, Wei‐min
- Subjects
ACADEMIC medical centers ,APOPTOSIS ,CARRIER proteins ,CELL culture ,CHEMOKINES ,IMMUNE system ,INFLAMMATION ,INTERLEUKINS ,LUNG cancer ,LUNG tumors ,POLYMERASE chain reaction ,RESEARCH funding ,T-test (Statistics) ,WESTERN immunoblotting ,REVERSE transcriptase polymerase chain reaction ,DATA analysis software - Abstract
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. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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