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LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression

HCC is one of the most common malignant tumors worldwide. Although traditional treatment methods have been improved in recent years, the survival rate of HCC patients has not been significantly improved. Immunotherapy has shown extremely high clinical value in a variety of tumors. In this study, we...

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Autores principales: Wu, Rongshou, Liu, Weiwei, Yang, Qingping, Zhang, Jingling, Hou, Ping, Xiong, Jianghui, Wu, Linquan, Li, Enliang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10562488/
https://www.ncbi.nlm.nih.gov/pubmed/37813900
http://dx.doi.org/10.1038/s41598-023-42948-8
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author Wu, Rongshou
Liu, Weiwei
Yang, Qingping
Zhang, Jingling
Hou, Ping
Xiong, Jianghui
Wu, Linquan
Li, Enliang
author_facet Wu, Rongshou
Liu, Weiwei
Yang, Qingping
Zhang, Jingling
Hou, Ping
Xiong, Jianghui
Wu, Linquan
Li, Enliang
author_sort Wu, Rongshou
collection PubMed
description HCC is one of the most common malignant tumors worldwide. Although traditional treatment methods have been improved in recent years, the survival rate of HCC patients has not been significantly improved. Immunotherapy has shown extremely high clinical value in a variety of tumors. In this study, we found that TUG1 could regulate the expression of PD-L1 through JAK2/STAT3 to mediate immunosuppression. Here, The expression of TUG1 and PD-L1 in HCC tissues was evaluated through analysis of databases and verified in HCC tissue and HCC cancer cells by qRT-PCR. The effect of TUG1 on tumor immune escape was detected by coculture, and cell viability was detected with a CCK8 assay. The results demonstrated that TUG1 was closely associated with anticancer immunity. TUG1 and PD-L1 were highly expressed in HCC tissues and HCC cancer cells, and high expression of TUG1 and PD-L1 was related to the poor prognosis of HCC patients. In addition, knocking down TUG1 expression could reduce PD-L1 expression and enhance the cancer cell-killing capability of T cells. Downregulating TUG1 expression could also decrease the mRNA and protein expression of JAK2 and STAT3. To sum up, TUG1 and PD-L1 are overexpressed in patients with liver cancer and are related to the poor prognosis of these patients. Silencing TUG1 expression reduced the mRNA and protein expression of PD-L1 by affecting the JAK2/STAT3 pathway.
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spelling pubmed-105624882023-10-11 LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression Wu, Rongshou Liu, Weiwei Yang, Qingping Zhang, Jingling Hou, Ping Xiong, Jianghui Wu, Linquan Li, Enliang Sci Rep Article HCC is one of the most common malignant tumors worldwide. Although traditional treatment methods have been improved in recent years, the survival rate of HCC patients has not been significantly improved. Immunotherapy has shown extremely high clinical value in a variety of tumors. In this study, we found that TUG1 could regulate the expression of PD-L1 through JAK2/STAT3 to mediate immunosuppression. Here, The expression of TUG1 and PD-L1 in HCC tissues was evaluated through analysis of databases and verified in HCC tissue and HCC cancer cells by qRT-PCR. The effect of TUG1 on tumor immune escape was detected by coculture, and cell viability was detected with a CCK8 assay. The results demonstrated that TUG1 was closely associated with anticancer immunity. TUG1 and PD-L1 were highly expressed in HCC tissues and HCC cancer cells, and high expression of TUG1 and PD-L1 was related to the poor prognosis of HCC patients. In addition, knocking down TUG1 expression could reduce PD-L1 expression and enhance the cancer cell-killing capability of T cells. Downregulating TUG1 expression could also decrease the mRNA and protein expression of JAK2 and STAT3. To sum up, TUG1 and PD-L1 are overexpressed in patients with liver cancer and are related to the poor prognosis of these patients. Silencing TUG1 expression reduced the mRNA and protein expression of PD-L1 by affecting the JAK2/STAT3 pathway. Nature Publishing Group UK 2023-10-09 /pmc/articles/PMC10562488/ /pubmed/37813900 http://dx.doi.org/10.1038/s41598-023-42948-8 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Wu, Rongshou
Liu, Weiwei
Yang, Qingping
Zhang, Jingling
Hou, Ping
Xiong, Jianghui
Wu, Linquan
Li, Enliang
LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression
title LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression
title_full LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression
title_fullStr LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression
title_full_unstemmed LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression
title_short LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression
title_sort lnctug1 promotes hepatocellular carcinoma immune evasion via upregulating pd-l1 expression
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10562488/
https://www.ncbi.nlm.nih.gov/pubmed/37813900
http://dx.doi.org/10.1038/s41598-023-42948-8
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