Does burning fat make tumor immune hot? Discovery of CD47 overexpression by radiation induced fatty acid oxidation

Nian Jiang; Bowen Xie; Ming Fan; Jian Jian Li

doi:10.1016/j.gendis.2022.07.019

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Does burning fat make tumor immune hot? Discovery of CD47 overexpression by radiation induced fatty acid oxidation

更新时间：2023-08-29

- Does burning fat make tumor immune hot? Discovery of CD47 overexpression by radiation induced fatty acid oxidation
- Genes & Diseases Vol. 10, Issue 1, (2023)
- 作者机构：
  
  1. Department of Radiation Oncology, University of California Davis School of Medicine, Sacramento,CA,USA,95817
  2. Department of Neurosurgery, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University,Hunan,Changsha,China,410008
  3. Institute for Immunology and School of Medicine, Tsinghua University,Beijing,China,100084
  4. NCI-Designated Comprehensive Cancer Center, University of California Davis, Sacramento,CA,USA,95817
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2022.07.019
  CLC：
- Published：2023，
  
  Published Online：1 January 2023，
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Nian Jiang, Bowen Xie, Ming Fan, et al. Does burning fat make tumor immune hot? Discovery of CD47 overexpression by radiation induced fatty acid oxidation. [J]. Genes & Diseases 10(1).(2023)
DOI：

Nian Jiang, Bowen Xie, Ming Fan, et al. Does burning fat make tumor immune hot? Discovery of CD47 overexpression by radiation induced fatty acid oxidation. [J]. Genes & Diseases 10(1).(2023) DOI： 10.1016/j.gendis.2022.07.019.

摘要

Abstract

lthough extensively studied

it is unknown what is the major cellular energy driving tumor metastasis after anti-cancer radiotherapy. Metabolic reprogramming is one of the fundamental hallmarks in carcinogenesis and tumor progression featured with the increased glycolysis in solid tumors. However

accumulating evidence indicates that in addition to the rudimentary glycolytic pathway

tumor cells are capable of reactivating mitochondrial OXPHOS under genotoxic stress condition to meet the increasing cellular fuel demand for repairing and surviving anti-cancer radiation. Such dynamic metabolic rewiring may play a key role in cancer therapy resistance and metastasis. Interestingly

data from our group and others have demonstrated that cancer cells can re-activate mitochondrial oxidative respiration to boost an annexing energy to meet the increasing cellular fuel demand for tumor cells surviving genotoxic anti-cancer therapy with metastatic potential.

关键词

Keywords

CD47Immune checkpointImmunotherapyMetabolic rewiringRadiation therapyTumor acquired resistance

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