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Sonocavitation-Induced Mitochondrial Dysfunction via ROS-Mediated Apoptosis for Paclitaxel-Resistant Ovarian Cancer

Jian Qiu1, Zhikang Xu2, Xiaodong Wu2

  • 1Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China; Department of Obstetrics and Gynaecology, Huzhou Central Hospital, Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, Affiliated Central Hospital Huzhou University, Huzhou, China.

Ultrasound in Medicine & Biology
|January 13, 2026
PubMed
Summary

Sonocavitation overcomes paclitaxel resistance in ovarian cancer by inducing apoptosis via reactive oxygen species (ROS)-mediated mitochondrial dysfunction. This ultrasound therapy shows promise for enhancing treatment outcomes.

Keywords:
Low-intensity focused ultrasoundMicrobubblesMitochondriaOvarian cancerSonocavitation

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Area of Science:

  • Biomedical Engineering
  • Oncology
  • Cell Biology

Background:

  • Paclitaxel resistance is a major challenge in ovarian cancer treatment.
  • Ovarian cancer cells can develop resistance to paclitaxel, limiting therapeutic efficacy.
  • Understanding the mechanisms of chemoresistance is crucial for developing new treatment strategies.

Purpose of the Study:

  • To investigate if sonocavitation can overcome paclitaxel resistance in ovarian cancer.
  • To determine if sonocavitation promotes apoptosis through reactive oxygen species (ROS)-mediated mitochondrial dysfunction.
  • To evaluate the in vivo efficacy and safety of sonocavitation in paclitaxel-resistant ovarian cancer models.

Main Methods:

  • Compared apoptosis-related protein expression in resistant vs. sensitive ovarian cancer cells.
  • Applied sonocavitation to resistant cells and assessed apoptosis, ROS production, and mitochondrial function.
  • Utilized flow cytometry, electron microscopy, Western blotting, and in vivo xenograft models for evaluation.

Main Results:

  • Sonocavitation significantly increased apoptosis in paclitaxel-resistant ovarian cancer cells.
  • Induced mitochondrial dysfunction, including reduced ATP and membrane potential, and cytochrome c release.
  • Suppressed tumor growth and prolonged survival in vivo without systemic toxicity, with ROS playing a key mediator role.

Conclusions:

  • Sonocavitation effectively induces apoptosis in paclitaxel-resistant ovarian cancer via ROS-mediated mitochondrial dysfunction.
  • Demonstrates significant tumor-suppressive activity and a favorable safety profile.
  • Represents a promising adjuvant strategy to overcome chemoresistance and improve ovarian cancer treatment.