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Glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells

Hepatocellular carcinoma (HCC) is a complex process that plays an important role in its progression. Abnormal glucose metabolism in HCC cells can meet the nutrients required for the occurrence and development of liver cancer, better adapt to changes in the surrounding microenvironment, and escape th...

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Detalles Bibliográficos
Autores principales: Zhang, Qiuyue, Liu, Jinchen, Lin, Haifeng, Lin, Bo, Zhu, Mingyue, Li, Mengsen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Open Exploration Publishing 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10344893/
https://www.ncbi.nlm.nih.gov/pubmed/37455832
http://dx.doi.org/10.37349/etat.2023.00149
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author Zhang, Qiuyue
Liu, Jinchen
Lin, Haifeng
Lin, Bo
Zhu, Mingyue
Li, Mengsen
author_facet Zhang, Qiuyue
Liu, Jinchen
Lin, Haifeng
Lin, Bo
Zhu, Mingyue
Li, Mengsen
author_sort Zhang, Qiuyue
collection PubMed
description Hepatocellular carcinoma (HCC) is a complex process that plays an important role in its progression. Abnormal glucose metabolism in HCC cells can meet the nutrients required for the occurrence and development of liver cancer, better adapt to changes in the surrounding microenvironment, and escape the attack of the immune system on the tumor. There is a close relationship between reprogramming of glucose metabolism and immune escape. This article reviews the current status and progress of glucose metabolism reprogramming in promoting immune escape in liver cancer, aiming to provide new strategies for clinical immunotherapy of liver cancer.
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spelling pubmed-103448932023-07-15 Glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells Zhang, Qiuyue Liu, Jinchen Lin, Haifeng Lin, Bo Zhu, Mingyue Li, Mengsen Explor Target Antitumor Ther Review Hepatocellular carcinoma (HCC) is a complex process that plays an important role in its progression. Abnormal glucose metabolism in HCC cells can meet the nutrients required for the occurrence and development of liver cancer, better adapt to changes in the surrounding microenvironment, and escape the attack of the immune system on the tumor. There is a close relationship between reprogramming of glucose metabolism and immune escape. This article reviews the current status and progress of glucose metabolism reprogramming in promoting immune escape in liver cancer, aiming to provide new strategies for clinical immunotherapy of liver cancer. Open Exploration Publishing 2023 2023-06-30 /pmc/articles/PMC10344893/ /pubmed/37455832 http://dx.doi.org/10.37349/etat.2023.00149 Text en © The Author(s) 2023. https://creativecommons.org/licenses/by/4.0/This is an Open Access article licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review
Zhang, Qiuyue
Liu, Jinchen
Lin, Haifeng
Lin, Bo
Zhu, Mingyue
Li, Mengsen
Glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells
title Glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells
title_full Glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells
title_fullStr Glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells
title_full_unstemmed Glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells
title_short Glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells
title_sort glucose metabolism reprogramming promotes immune escape of hepatocellular carcinoma cells
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10344893/
https://www.ncbi.nlm.nih.gov/pubmed/37455832
http://dx.doi.org/10.37349/etat.2023.00149
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