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Oxidative Phosphorylation Inhibition...

Betancourt Ponce, Mayra A.,

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Oxidative Phosphorylation Inhibition in Solid Tumors /

Record Type:	Electronic resources : Monograph/item
Title/Author:	Oxidative Phosphorylation Inhibition in Solid Tumors // Mayra A Betancourt Ponce.
Author:	Betancourt Ponce, Mayra A.,
Description:	1 electronic resource (169 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 86-09, Section: B.
Contained By:	Dissertations Abstracts International86-09B.
Subject:	Oncology. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31847416
ISBN:	9798310146327

Oxidative Phosphorylation Inhibition in Solid Tumors /
Betancourt Ponce, Mayra A.,

Oxidative Phosphorylation Inhibition in Solid Tumors /Mayra A Betancourt Ponce. - 1 electronic resource (169 pages)

Source: Dissertations Abstracts International, Volume: 86-09, Section: B.

Oxidative phosphorylation (OXPHOS) is the primary metabolic pathway through which normal cells produce energy. In contrast, cancer cells have long been thought to rely on aerobic glycolysis for rapid energy production and proliferation, an observation that has led to OXPHOS being underexplored as a therapeutic target. However, the rise of the oncometabolism field over the past few decades has revealed that tumors can exploit different metabolic pathways, including OXPHOS, as disease progresses. Notably, OXPHOS has been linked to key protumorigenic properties, such as metastatic potential and chemoresistance. This thesis investigates OXPHOS inhibition as a therapeutic strategy using the FDA-approved agent atovaquone, which offers a safe toxicity profile compared to other OXPHOS inhibitors that have shown high toxicity in clinical trials. In epithelial ovarian cancer, the deadliest gynecologic cancer, atovaquone has shown promising results, including reduced tumor weights and ascites volumes. However, its precise mechanisms and full range of molecular effects are poorly understood. Through a transcriptomic approach and validation studies, we demonstrate that atovaquone not only disrupts cellular metabolism but also activates stress responses and primes ovarian cancer cells for immune recognition. In melanoma, although OXPHOS has been implicated in disease progression, atovaquone's effects have not been explored, making this study the first to evaluate its antitumorigenic effects in this context. Altogether, these findings offer new insights into the mechanisms of atovaquone across different solid tumor models. This work highlights OXPHOS inhibition as a promising and feasible therapeutic strategy, contributing to the rapidly expanding field of oncometabolism.

English

ISBN: 9798310146327Subjects--Topical Terms:

751006
Oncology.
Subjects--Index Terms:

Atovaquone

Oxidative Phosphorylation Inhibition in Solid Tumors /
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520 $a Oxidative phosphorylation (OXPHOS) is the primary metabolic pathway through which normal cells produce energy. In contrast, cancer cells have long been thought to rely on aerobic glycolysis for rapid energy production and proliferation, an observation that has led to OXPHOS being underexplored as a therapeutic target. However, the rise of the oncometabolism field over the past few decades has revealed that tumors can exploit different metabolic pathways, including OXPHOS, as disease progresses. Notably, OXPHOS has been linked to key protumorigenic properties, such as metastatic potential and chemoresistance. This thesis investigates OXPHOS inhibition as a therapeutic strategy using the FDA-approved agent atovaquone, which offers a safe toxicity profile compared to other OXPHOS inhibitors that have shown high toxicity in clinical trials. In epithelial ovarian cancer, the deadliest gynecologic cancer, atovaquone has shown promising results, including reduced tumor weights and ascites volumes. However, its precise mechanisms and full range of molecular effects are poorly understood. Through a transcriptomic approach and validation studies, we demonstrate that atovaquone not only disrupts cellular metabolism but also activates stress responses and primes ovarian cancer cells for immune recognition. In melanoma, although OXPHOS has been implicated in disease progression, atovaquone's effects have not been explored, making this study the first to evaluate its antitumorigenic effects in this context. Altogether, these findings offer new insights into the mechanisms of atovaquone across different solid tumor models. This work highlights OXPHOS inhibition as a promising and feasible therapeutic strategy, contributing to the rapidly expanding field of oncometabolism.
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650 4 $a Pathology. $3 643180
650 4 $a Molecular biology. $3 517296
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