Mitochondrial metabolism and cancer
By P. Porporato, N. Filigheddu, J. B. Pedro, Guido Kroemer, L. Galluzzi. Cell Research, 2017
1,145 citations recorded by the source corpus.
Glycolysis has long been considered as the major metabolic process for energy production and anabolic growth in cancer cells. Although such a view has been instrumental for the development of powerful imaging tools that are still used in the clinics, it is now clear that mitochondria play a key role in oncogenesis. Besides exerting central bioenergetic functions, mitochondria provide indeed building blocks for tumor anabolism, control redox and calcium homeostasis, participate in transcriptional regulation, and govern cell death. Thus, mitochondria constitute promising targets for the development of novel anticancer agents. However, tumors arise, progress, and respond to therapy in the context of an intimate crosstalk with the host immune system, and many immunological functions rely on intact mitochondrial metabolism. Here, we review the cancer cell-intrinsic and cell-extrinsic mechanisms through which mitochondria influence all steps of oncogenesis, with a focus on the therapeutic potential of targeting mitochondrial metabolism for cancer therapy.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/582929122f2c1df1785647ad5baa101db7d8d97c
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In Cancer Research
In Molecular Biology
Citations in the corpus
- Cuproptosis: mechanisms and links with cancers (2023, background): “Certain tumors inherently exhibit higher levels of mitochondrial metabolism, such as melanoma, breast cancer and leukemia [5].”
- Flavonoids as Anticancer Agents (2020, background): “Tumor-cell metabolism is altered compared to normal cells due to highly abnormal mitochondrial functions (Figure 8) [171].”
- Packaging and transfer of mitochondrial DNA via exosomes regulate escape from dormancy in hormonal therapy-resistant breast cancer (2017, positive): “These mutations may represent passenger events during therapy-driven cancer cell selection (39); alternatively, when accumulating toward homoplasmy, they may be drivers of disease (40), playing a prominent role in chemoresistance.”