Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Sep 6:12:971479.
doi: 10.3389/fonc.2022.971479. eCollection 2022.

Targeting oxidative phosphorylation as an approach for the treatment of ovarian cancer

Affiliations
Review

Targeting oxidative phosphorylation as an approach for the treatment of ovarian cancer

Yinjie Wu et al. Front Oncol. .

Abstract

Ovarian cancer is an aggressive tumor that remains to be the most lethal gynecological malignancy in women. Metabolic adaptation is an emerging hallmark of tumors. It is important to exploit metabolic vulnerabilities of tumors as promising strategies to develop more effective anti-tumor regimens. Tumor cells reprogram the metabolic pathways to meet the bioenergetic, biosynthetic, and mitigate oxidative stress required for tumor cell proliferation and survival. Oxidative phosphorylation has been found to be altered in ovarian cancer, and oxidative phosphorylation is proposed as a therapeutic target for management of ovarian cancer. Herein, we initially introduced the overview of oxidative phosphorylation in cancer. Furthermore, we discussed the role of oxidative phosphorylation and chemotherapeutic resistance of ovarian cancer. The role of oxidative phosphorylation in other components of tumor microenvironment of ovarian cancer has also been discussed.

Keywords: metabolic reprograming; mitochondria; ovarian cancer; oxidative phoshorylation; resistance.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Illustration of mitochondrial electron transport, oxygen consumption and OXPHOS in cells.
Figure 2
Figure 2
Illustration of oxidative phosphorylation and chemotherapeutic resistance of ovarian tumors. OXPHOS, oxidative phosphorylation; ETC, electron transport chain.

Similar articles

Cited by

References

    1. Webb PM, Jordan SJ. Epidemiology of epithelial ovarian cancer. Best Pract Res Clin Obstet. Gynaecol. (2017) 41:3–14. doi: 10.1016/j.bpobgyn.2016.08.006 - DOI - PubMed
    1. Li SS, Ma J, Wong AST. Chemoresistance in ovarian cancer: Exploiting cancer stem cell metabolism. J Gynecol. Oncol (2018) 29(2):e32. doi: 10.3802/jgo.2018.29.e32 - DOI - PMC - PubMed
    1. Vander Heiden MG, DeBerardinis RJ. Understanding the intersections between metabolism and cancer biology. Cell (2017) 168(4):657–69. doi: 10.1016/j.cell.2016.12.039 - DOI - PMC - PubMed
    1. Dey P, Kimmelman AC, DePinho RA. Metabolic codependencies in the tumor microenvironment. Cancer Discovery (2021) 11(5):1067–81. doi: 10.1158/2159-8290.CD-20-1211 - DOI - PMC - PubMed
    1. Martínez-Reyes I, Chandel NS. Cancer metabolism: Looking forward. Nat Rev Cancer (2021) 21(10):669–80. doi: 10.1038/s41568-021-00378-6 - DOI - PubMed

LinkOut - more resources