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REVIEW article

Front. Pharmacol.

Sec. Translational Pharmacology

This article is part of the Research TopicEmerging Targeted and Immunotherapeutic Strategies in Oncology: From Solid Tumors to Hematologic MalignanciesView all 9 articles

Mitochondrial Involvement in PC: Improving Therapeutic Strategies

Provisionally accepted
Jiaxin  ZhangJiaxin Zhang1Chang  LouChang Lou2,3*
  • 1Beilun District People's Hospital, beilun, China
  • 2Second People's Hospital of Beilun District, Ningbo, China
  • 3Beilun District People's Hospital, ningbo, China

The final, formatted version of the article will be published soon.

Abstract Prostate cancer (PC) is a complex disease propelled by various molecular mechanisms. The role of mitochondria in PC has recently emerged as a significant research focus. Mitochondria, often referred to as the cell's powerhouses, are not only essential for energy production but also crucial for key cellular processes like apoptosis, oxidative stress, and metabolic reprogramming. Changes in energy metabolism, marked by an increased dependency on oxidative phosphorylation (OXPHOS), have been noted in PC cells, offering a potential therapeutic target. Moreover, specific mitochondrial DNA (mtDNA) mutations have been linked with advanced tumors and adverse patient outcomes in PC. The mitochondrial reactive oxygen species (ROS), the disruption of mitochondrial dynamics and the fine balance between pro-apoptotic and anti-apoptotic signals mediated by Bcl-2 family proteins have also been implicated in PC. Comprehending the complex interaction between mitochondria and PC biology offers substantial potential for creating innovative targeted therapeutic strategies. This review emphasizes the role of mitochondria in the occurrence and malignant progression of PC, as well as the potential of targeted interventions on mitochondria in developing treatments, which may improve the prognosis of PC patients.

Keywords: prostate cancer, Oxidative Phosphorylation, mitochondria DNA, reactiveoxygen species, Membrane permeabilization, Apoptosis, mitochondrial dynamics

Received: 22 Sep 2025; Accepted: 24 Oct 2025.

Copyright: © 2025 Zhang and Lou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Chang Lou, louchang5753@163.com

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