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Long Noncoding RNA GM16343 Promotes IL-36ß to Regulate Tumor Microenvironment by CD8+T cells.
Technol Cancer Res Treat ; 18: 1533033819883633, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31684829


To investigate the effect of long noncoding RNA GM16343 on interleukin 36ß promotion of CD8+T cells in tumor microenvironment regulation.


The differentially expressed long noncoding RNA in interleukin 36ß-stimulated mouse CD8+T cells was screened by gene chip technology, and the significant differentially expressed long noncoding RNAs were verified by real-time polymerase chain reaction. The lentiviral vector that overexpresses or knockdown GM16343 was constructed, transfected into CD8+T cells, and stimulated with interleukin 36ß, and the amount of interferon γ secreted was detected by enzyme-linked immunosorbent assay. A mouse subcutaneous xenograft model that stably express interleukin 36ß was established, and the tumor size and mouse survival time were observed by stimulation with CD8+T cells overexpression or knockdown of GM16343.


A total of 12 long noncoding RNAs with significant differences were screened by gene chip analysis. Real-time polymerase chain reaction showed that the difference in GM16343 was larger, and the difference between the groups was observed to be the most significant. Compared to control group, CD8+T cells overexpressing GM16343 increased the secretion of interferon γ, and the tumor diameter of the mice after stimulation showed significant reduction, and the survival time showed significant prolongation. Compared to control group, the CD8+T cells after GM16343 were knocked down. The interferon γ secretion was decreased, and no significant change in tumor diameter and survival time was observed.


Interleukin 36ß may enhance antitumor immune response of CD8+T cells by regulating GM16343.





Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Idioma: Inglês Revista: Technol Cancer Res Treat Assunto da revista: Neoplasias / Terapêutica Ano de publicação: 2019 Tipo de documento: Artigo País de afiliação: China