» Articles » PMID: 33834022

Cell Metabolism and DNA Repair Pathways: Implications for Cancer Therapy

Overview
Specialty Cell Biology
Date 2021 Apr 9
PMID 33834022
Citations 30
Authors
Affiliations
Soon will be listed here.
Abstract

DNA repair and metabolic pathways are vital to maintain cellular homeostasis in normal human cells. Both of these pathways, however, undergo extensive changes during tumorigenesis, including modifications that promote rapid growth, genetic heterogeneity, and survival. While these two areas of research have remained relatively distinct, there is growing evidence that the pathways are interdependent and intrinsically linked. Therapeutic interventions that target metabolism or DNA repair systems have entered clinical practice in recent years, highlighting the potential of targeting these pathways in cancer. Further exploration of the links between metabolic and DNA repair pathways may open new therapeutic avenues in the future. Here, we discuss the dependence of DNA repair processes upon cellular metabolism; including the production of nucleotides required for repair, the necessity of metabolic pathways for the chromatin remodeling required for DNA repair, and the ways in which metabolism itself can induce and prevent DNA damage. We will also discuss the roles of metabolic proteins in DNA repair and, conversely, how DNA repair proteins can impact upon cell metabolism. Finally, we will discuss how further research may open therapeutic avenues in the treatment of cancer.

Citing Articles

Hypoxia Dependent Inhibition of Glioblastoma Cell Proliferation, Invasion, and Metabolism by the Choline-Kinase Inhibitor JAS239.

Kelly C, Wydrzynska M, Phelan M, Osharovich S, Delikatny E, See V Metabolites. 2025; 15(2).

PMID: 39997701 PMC: 11857610. DOI: 10.3390/metabo15020076.


DNA replication initiation drives focal mutagenesis and rearrangements in human cancers.

Murat P, Guilbaud G, Sale J Nat Commun. 2024; 15(1):10850.

PMID: 39738026 PMC: 11685606. DOI: 10.1038/s41467-024-55148-3.


PINK1-Mediated Mitochondrial Activity Confers Olaparib Resistance in Prostate Cancer Cells.

Schaaf Z, Ning S, Leslie A, Sharifi M, Gao R, Maine J Cancer Res Commun. 2024; 4(11):2976-2985.

PMID: 39440945 PMC: 11577557. DOI: 10.1158/2767-9764.CRC-24-0339.


Heterojunction semiconductor nanocatalysts as cancer theranostics.

Sabu A, Kandel M, Sarma R, Ramesan L, Roy E, Sharmila R APL Bioeng. 2024; 8(4):041502.

PMID: 39381587 PMC: 11459490. DOI: 10.1063/5.0223718.


Impact of genetic variants in the solute carrier () genes encoding drug uptake transporters on the response to anticancer chemotherapy.

Marin J, Serrano M, Herraez E, Lozano E, Ortiz-Rivero S, Perez-Silva L Cancer Drug Resist. 2024; 7:27.

PMID: 39143954 PMC: 11322974. DOI: 10.20517/cdr.2024.42.


References
1.
Koerner S, Hanai J, Bai S, Jernigan F, Oki M, Komaba C . Design and synthesis of emodin derivatives as novel inhibitors of ATP-citrate lyase. Eur J Med Chem. 2016; 126:920-928. DOI: 10.1016/j.ejmech.2016.12.018. View

2.
Yalcin A, Telang S, Clem B, Chesney J . Regulation of glucose metabolism by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases in cancer. Exp Mol Pathol. 2009; 86(3):174-9. DOI: 10.1016/j.yexmp.2009.01.003. View

3.
Sharma N, Lebedeva M, Thomas T, Kovalenko O, Stumpf J, Shadel G . Intrinsic mitochondrial DNA repair defects in Ataxia Telangiectasia. DNA Repair (Amst). 2013; 13:22-31. PMC: 6211587. DOI: 10.1016/j.dnarep.2013.11.002. View

4.
Lieber M . The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway. Annu Rev Biochem. 2010; 79:181-211. PMC: 3079308. DOI: 10.1146/annurev.biochem.052308.093131. View

5.
Warburg O, Wind F, Negelein E . THE METABOLISM OF TUMORS IN THE BODY. J Gen Physiol. 2009; 8(6):519-30. PMC: 2140820. DOI: 10.1085/jgp.8.6.519. View