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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Updated: Sep 15, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
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Mitochondria-Targeted Antibiotics toward Drug Resistant TNBC.

Miae Won1,2, Changyu Yoon3, Jusung An3

  • 1College of Pharmacy, Dongduk Women's University, Seoul 02748, Korea.

ACS Applied Bio Materials
|July 16, 2025
PubMed
Summary

A novel mitochondria-targeted antibiotic, compound 1 (CFX-TPP+), shows promise in overcoming drug resistance in triple-negative breast cancer (TNBC). It enhances reactive oxygen species (ROS) generation, inducing cancer cell death and potentially offering a cure without relapse.

Keywords:
AntibioticsAnticancer DrugDrug ResistanceMitochondriaMitochondrial Cell DeathReactive Oxygen SpeciesTriple-Negative Breast Cancer

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Drug resistance poses a significant challenge in cancer therapy.
  • Mitochondria are key regulators of cell survival and death via reactive oxygen species (ROS).
  • Targeting mitochondria offers a strategy to enhance cancer treatment efficacy and overcome resistance.

Purpose of the Study:

  • To introduce and evaluate a novel mitochondria-targeted antibiotic, compound 1 (CFX-TPP+), for combating drug-resistant triple-negative breast cancer (TNBC).
  • To assess the stability and in vitro efficacy of compound 1 against TNBC cells.

Main Methods:

  • Synthesis and characterization of compound 1 (CFX-TPP+), a mitochondria-targeted antibiotic with an amide functional unit.
  • Assessment of compound 1's stability in blood plasma compared to an ester-containing analog.
  • Evaluation of compound 1's cytotoxicity against drug-resistant TNBC cells (MDA-MB-231).
  • Analysis of ROS generation, mitochondrial oxidative stress, and downstream apoptotic signaling pathways.

Main Results:

  • Compound 1 demonstrated superior stability in blood plasma compared to its ester counterpart.
  • Compound 1 exhibited significant cytotoxicity against drug-resistant TNBC cells.
  • Treatment with compound 1 led to enhanced ROS generation and increased mitochondrial oxidative stress.
  • Compound 1 induced mitochondria-mediated apoptosis, upregulated BAX, and downregulated genes involved in mitochondrial biogenesis.

Conclusions:

  • Compound 1 (CFX-TPP+) is a stable and effective mitochondria-targeted agent against drug-resistant TNBC.
  • This approach shows potential for overcoming drug resistance and achieving disease remission in TNBC.
  • Targeting mitochondrial ROS offers a promising strategy for novel cancer therapeutics.