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Updated: Oct 2, 2025
Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
ROS-Induced DCTPP1 Upregulation Contributes to Cisplatin Resistance in Ovarian Cancer
Yu Wang1, Peishi Chen2, Xueping Chen1
1Obstetrics and Gynecology Center, Nanfang Hospital, Guangzhou, China.
Abstract:
Cisplatin resistance hinders the improvement of the prognosis of patients with ovarian cancer. Cisplatin induces cancer cell apoptosis by inducing reactive oxygen species (ROS). dCTP pyrophosphatase 1 (DCTPP1) is a newly discovered dNTP pyrophosphatase. This study aimed to identify the role of DCTPP1 in oxidative stress and cisplatin response of ovarian cancer. Our results indicates cisplatin-induced ROS generation was responsible for the upregulation of DCTPP1 in ovarian cancer cells, whereas DCTPP1 knockdown significantly enhanced the sensitivity of ovarian cancer cells to cisplatin, reflect in reactive oxygen species (ROS) generation, double-strand DNA breaks, and cell apoptosis. The expression of redox-related genes and the activation of the PI3/Akt signaling pathway were also inhibited by DCTPP1 knockdown. Our data proposes that the development of therapeutic approaches targeting DCTPP1 may be useful in the treatment of ovarian cancer.
Insights
Targeting dCTP pyrophosphatase 1 (DCTPP1) may improve ovarian cancer treatment. Inhibiting DCTPP1 enhances cisplatin sensitivity by increasing oxidative stress and apoptosis, offering new therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Cisplatin resistance is a major challenge in ovarian cancer treatment.
- Cisplatin induces apoptosis via reactive oxygen species (ROS).
- dCTP pyrophosphatase 1 (DCTPP1) is a novel dNTP pyrophosphatase.
Purpose of the Study:
- To investigate the role of DCTPP1 in ovarian cancer's response to cisplatin and oxidative stress.
- To explore DCTPP1 as a potential therapeutic target.
Main Methods:
- Ovarian cancer cell lines were treated with cisplatin.
- DCTPP1 expression was analyzed.
- DCTPP1 knockdown was performed using siRNA.
- ROS generation, DNA damage, apoptosis, redox gene expression, and PI3K/Akt pathway activation were assessed.
Main Results:
- Cisplatin treatment upregulated DCTPP1 expression in ovarian cancer cells, correlating with ROS generation.
- DCTPP1 knockdown significantly increased ovarian cancer cell sensitivity to cisplatin.
- Knockdown of DCTPP1 enhanced ROS production, double-strand DNA breaks, and apoptosis.
- DCTPP1 inhibition suppressed redox-related gene expression and PI3K/Akt pathway activation.
Conclusions:
- DCTPP1 plays a crucial role in mediating cisplatin resistance in ovarian cancer.
- Targeting DCTPP1 could be a promising strategy to overcome cisplatin resistance and improve treatment outcomes for ovarian cancer patients.
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