Related Experiment Video
Updated: Feb 20, 2026
Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
Mir-29b Regulates Oxidative Stress by Targeting SIRT1 in Ovarian Cancer Cells
Meng Hou1, Xiaohang Zuo2, Chen Li1
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Background:
Metabolic abnormalities are frequently observed in multiple malignancies including epithelial ovarian cancer (EOC), among which imbalance between generation and elimination of reactive oxygen species (ROS) plays a critical role in EOC onset and progression. Here we investigated the role of miR-29b, a well-established tumor-suppressor miRNA in metabolic regulation of EOC cells.
Methods:
cell viability and apoptosis in miR-29b inhibited and over-expressed EOC cells were evaluated by CCK8 and Annexin V-FITC/PI assays. Change in miR-29b was detected in EOC cells incubated in H2O2 culture by q-PCR. Relative ROS levels were also detected in different EOC cultures, including modified miR-29b and SIRT1 levels as well as H2O2 incubation. A luciferase reporter assay was employed to detect the direct binding of miR-29b to SIRT1 3' UTR. Changes in cell viability and ROS levels were assessed in SIRT1-knocked down EOC cells.
Results:
miR-29b expression correlates with decreased EOC cell viability and increased apoptosis. H2O2 downregulated miR-29b in a time and dose-dependent manner. miR-29b expression negatively correlated with ROS levels, whereas SIRT1 significantly stimulated ROS formation. Luciferase reporter assays confirmed miR-29b downregulation of SIRT1by directly targeting its mRNA 3'-UTR. SIRT1 silencing rescues cell viability of H2O2 treated cells. Also, SIRT1 inhibition blocked cell apoptosis induced by H2O2 as well as reduced intracellular ROS levels.
Conclusion:
Together, our findings indicated that the miR-29b/SIRT1 axis has a protective effect against H2O2-induced damage of cell viability and oxidative stress and may provide novel options for miR-29b-based therapeutic approaches for EOC treatment.
Insights
MicroRNA-29b (miR-29b) protects epithelial ovarian cancer (EOC) cells from oxidative stress by downregulating SIRT1, thus reducing reactive oxygen species (ROS) and improving cell viability. This miR-29b/SIRT1 axis offers potential therapeutic strategies for EOC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Metabolic abnormalities and reactive oxygen species (ROS) imbalance are key in epithelial ovarian cancer (EOC) progression.
- MicroRNA-29b (miR-29b) is a known tumor suppressor involved in metabolic regulation within EOC cells.
Purpose of the Study:
- To investigate the role of miR-29b in the metabolic regulation of EOC cells.
- To elucidate the relationship between miR-29b, ROS, and SIRT1 in EOC.
Main Methods:
- Cell viability and apoptosis assays (CCK8, Annexin V-FITC/PI) were performed on EOC cells with altered miR-29b levels.
- Quantitative PCR (q-PCR) and ROS level detection were used to assess changes in miR-29b, SIRT1, and ROS.
- Luciferase reporter assays confirmed the direct binding of miR-29b to the SIRT1 3' UTR.
Main Results:
- miR-29b expression correlated with reduced EOC cell viability and increased apoptosis.
- Hydrogen peroxide (H2O2) downregulated miR-29b, which in turn negatively correlated with ROS levels.
- miR-29b directly targeted SIRT1 mRNA, and SIRT1 inhibition rescued cell viability and reduced ROS in H2O2-treated EOC cells.
Conclusions:
- The miR-29b/SIRT1 axis demonstrates a protective effect against H2O2-induced damage and oxidative stress in EOC.
- This axis presents potential therapeutic targets for miR-29b-based treatments in EOC.
Related Concept Videos
01:46Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...
01:24Peroxisomes