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Targeting Mitochondrial Metabolism to Reverse Radioresistance: An Alternative to Glucose Metabolism

期刊

ANTIOXIDANTS
卷 11, 期 11, 页码 -

出版社

MDPI
DOI: 10.3390/antiox11112202

关键词

radioresistance; reactive oxygen species; oxidative phosphorylation; oncometabolites; apoptosis

资金

  1. Jilin Provincial Science and Technology Foundations [20210509003RQ, 20210402002GH]
  2. Health Talents Special Project of the Jilin Provincial Finance Department [JLSWSRCZX2021-065]
  3. Changchun Science and Technology Development Plan [21ZY29]
  4. Achievement Transformation Guiding Foundations of the First Hospital of Jilin University [CGZHYD202012-029]

向作者/读者索取更多资源

Radiotherapy failure and poor tumor prognosis are mainly caused by radioresistance. The relationship and mechanisms between mitochondrial metabolism and cancer radioresistance are not fully understood. However, mitochondria play a crucial role in regulating various biological reactions and influencing the radiation effects of malignancies. Therefore, targeting mitochondrial signaling pathways for the development of novel anticancer drugs holds promise.
Radiotherapy failure and poor tumor prognosis are primarily attributed to radioresistance. Improving the curative effect of radiotherapy and delaying cancer progression have become difficult problems for clinicians. Glucose metabolism has long been regarded as the main metabolic process by which tumor cells meet their bioenergetic and anabolic needs, with the complex interactions between the mitochondria and tumors being ignored. This misconception was not dispelled until the early 2000s; however, the cellular molecules and signaling pathways involved in radioresistance remain incompletely defined. In addition to being a key metabolic site that regulates tumorigenesis, mitochondria can influence the radiation effects of malignancies by controlling redox reactions, participating in oxidative phosphorylation, producing oncometabolites, and triggering apoptosis. Therefore, the mitochondria are promising targets for the development of novel anticancer drugs. In this review, we summarize the internal relationship and related mechanisms between mitochondrial metabolism and cancer radioresistance, thus exploring the possibility of targeting mitochondrial signaling pathways to reverse radiation insensitivity. We suggest that attention should be paid to the potential value of mitochondria in prolonging the survival of cancer patients.

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