Related Experiment Video
Updated: Jan 15, 2026
Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence
Published on: November 2, 2014
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.
Objective:
To investigate whether sonocavitation, induced by low-intensity focused ultrasound combined with microbubbles, can overcome paclitaxel resistance in ovarian cancer by promoting apoptosis through reactive oxygen species (ROS)-mediated mitochondrial dysfunction.
Methods:
Paclitaxel-resistant ovarian cancer tissues and cell lines were compared with chemotherapy-sensitive counterparts for the expression of apoptosis-related proteins. Sonocavitation treatment was applied to resistant cells using optimized ultrasound parameters. Apoptosis, ROS production, mitochondrial morphology, oxygen consumption, mitochondrial membrane potential and mitochondrial membrane proteins were evaluated by flow cytometry, transmission electron microscopy, oxygen consumption assays, adenosine triphosphate (ATP) measurements, mitochondrial membrane potential assay kit staining and Western blotting. In vivo antitumor efficacy and biosafety were examined in paclitaxel-resistant xenograft mouse models, with tumor growth curves, survival analysis, and hematological/organ histology assessments.
Results:
Paclitaxel-resistant ovarian cancer tissues exhibited elevated Bcl-2 and reduced Bax and Caspase-3, indicating impaired intrinsic apoptosis. Sonocavitation significantly increased apoptosis in resistant ovarian cancer cells and induced marked mitochondrial dysfunction, including reduced mitochondrial size, disrupted oxygen consumption, decreased ATP levels, collapse of mitochondrial membrane potential and destruction of mitochondrial membrane proteins. Cytochrome c release and activation of cleaved Caspase-3 confirmed mitochondrial-dependent apoptosis. In vivo, sonocavitation suppressed tumor growth and prolonged survival without causing systemic toxicity. ROS scavengers partially reversed these effects, confirming that ROS accumulation is a key mediator of the therapeutic mechanism.
Conclusion:
Sonocavitation induces apoptosis in paclitaxel-resistant ovarian cancer through ROS-mediated mitochondrial dysfunction and demonstrates effective tumor-suppressive activity with a favorable safety profile. These findings support sonocavitation as a promising adjuvant strategy to overcome chemoresistance and enhance ovarian cancer treatment outcomes.
Insights
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.
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.
More Related Videos
Related Concept Videos
01:46Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
02:49Cancer Therapies
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
01:15Drugs that Stabilize Microtubules
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...