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Updated: Sep 6, 2025

Mitochondrial Respiration Quantification in Yeast Whole Cells
Published on: November 8, 2024
Resveratrol inhibits HeLa cell proliferation by regulating mitochondrial function
Yuming Zhang1, Fengyu Yuan2, Pei Li2
1The International Centre for Precision Environmental Health and Governance, College of Life Sciences, Hebei University, Baoding 071002, China; Key Laboratory of Zoological Systematics and Application of Hebei Province, College of Life Sciences, Hebei University, Baoding 071002, China.
Abstract:
The beneficial roles of resveratrol (RES) in affecting proliferation of multiple cancer cells have attracted intensive attention. However, the underlying mechanism remains unclear. This study aims to bridge the knowledge gap by investigating RES-induced growth inhibition of HeLa cells. Our work focuses on the metergasis of mitochondria in the RES-exposed cells. Therefore, HeLa cells were treated with different concentrations of RES for 30 min and 24 h, respectively. As a result, concentration-dependent increases in cell growth inhibition, ROS (reactive oxygen species) triggering, and LC3-II (light chain 3-II) expression were detected in the HeLa cells exposed to RES for 24 h. Interestingly, a specific concentration-dependent effect was observed in the HeLa cells exposed to RES for 30 min, that is, low concentration RES (≤ 25 μmol/L) reduced ROS levels, inhibited transcription and expression levels of LC3-II, and stimulated mitochondrial respiratory capacities. In contrast, high concentration RES (50 and 100 μmol/L) induced ROS over-production and autophagy in the cells, resulting in decreased levels of mitochondrial membrane potential, mitochondrial DNA copy numbers, and mitochondrial respiratory capacities. Together, our data concluded that RES inhibited HeLa cell proliferation through perturbation of mitochondrial structure and function, and ROS-induced autophagy also played a critical role in the process.
Insights
Resveratrol (RES) inhibits HeLa cancer cell proliferation by disrupting mitochondrial function. This process involves reactive oxygen species (ROS) and autophagy, highlighting RES as a potential anti-cancer agent.
Area of Science:
- Biochemistry
- Cell Biology
- Cancer Research
Background:
- Resveratrol (RES) shows promise in inhibiting cancer cell proliferation, but its precise mechanisms require further elucidation.
- Mitochondrial function and dynamics are critical in cellular processes, including cancer progression.
Purpose of the Study:
- To investigate the effects of resveratrol on HeLa cell proliferation.
- To explore the role of mitochondrial metergasis and reactive oxygen species (ROS) in resveratrol-induced growth inhibition.
Main Methods:
- HeLa cells were treated with varying concentrations of resveratrol for 30 minutes and 24 hours.
- Assessed cell growth inhibition, ROS levels, LC3-II expression, mitochondrial membrane potential, mitochondrial DNA copy numbers, and respiratory capacities.
Main Results:
- Resveratrol induced dose-dependent growth inhibition, ROS production, and LC3-II expression after 24 hours.
- Short-term (30 min) low-dose RES decreased ROS and LC3-II while enhancing mitochondrial respiration.
- Short-term high-dose RES triggered ROS overproduction, induced autophagy, and impaired mitochondrial function.
Conclusions:
- Resveratrol inhibits HeLa cell proliferation by perturbing mitochondrial structure and function.
- ROS-mediated autophagy plays a significant role in resveratrol's anti-cancer effects on HeLa cells.
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