Related Experiment Video
Updated: Aug 23, 2026
A Standardized Protocol for Inducing Stress-Induced Premature Senescence in Primary Human Melanocytes Using Tert-butyl Hydroperoxide
Published on: May 29, 2026
[p53-dependent antiproliferation and apoptosis of H22 cell induced by melatonin]
Mei-Hua She1, Bei-Bei Chen, Xi-Ming Wang
1Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P.R.China. shemh93013@hotmail.com
Background & Objective:
It has been shown that melatonin has a direct inhibitory effect on the proliferation of H22 mouse hepatoma cells in our research. This study was designed to investigate its molecular mechanism.
Methods:
(1) Animal models were established by transplanting H22 cells and treated with melatonin, and then the p53 and cyclin E of the tumor tissue were determined by immunohistochemical analysis. (2) After treatment of H22 cells with melatonin in vitro, the percentage of cells in each cell cycle phase and apoptosis rate were analyzed by flow cytometry. p53 and cyclin E were determined again by immunohistochemical analysis. The level of Fas mRNA was examined by real time polymerase chain reaction (RT-PCR).
Results:
(1) After treated with melatonin (1 x 10(-6) mol/L), the number of the H22 cells in phase G(0)/G(1) were elevated from 75.24% to 85.46%, while which in phase S almost decreased from 10.32% to 0, and at the same time, the number of apoptotic cells increased from 5.07% to 12.77%. (2) Compared with the control, the level of p53 elevated 42.5% (in vitro) and 19.5% (in vivo), however, the level of cyclin E decreased 31.7% (in vitro) and 39.9% (in vivo). (3) Fas mRNA increased about 44.2% after melatonin treatment (P< 0.01).
Conclusion:
Melatonin inhibits the proliferation of H22 cells by arrest and apoptosis, and the mechanism perhaps interferes with increasing p53 that results in down-regulation of cyclin E indirectly and stimulates the expression of Fas gene.
Insights
Melatonin effectively inhibits H22 hepatoma cell proliferation by inducing cell cycle arrest and apoptosis. This occurs through increased p53 levels, decreased cyclin E, and enhanced Fas gene expression.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Context:
- Hepatoma cell proliferation is a significant challenge in cancer research.
- Melatonin's anti-proliferative effects on cancer cells are increasingly recognized.
- Understanding the molecular pathways is crucial for therapeutic development.
Purpose:
- To elucidate the molecular mechanism by which melatonin inhibits H22 mouse hepatoma cell proliferation.
- To investigate the effects of melatonin on cell cycle distribution, apoptosis, and key protein/gene expression in H22 cells.
Summary:
- Melatonin treatment of H22 cells in vitro and in vivo led to increased G0/G1 phase arrest and apoptosis.
- Melatonin elevated p53 levels and Fas mRNA expression while decreasing cyclin E levels.
- These findings suggest melatonin's anti-proliferative action involves p53-mediated cyclin E downregulation and Fas gene stimulation.
Impact:
- Provides insights into melatonin's anti-cancer mechanisms in hepatoma.
- Identifies potential molecular targets for novel hepatoma therapies.
- Supports further research into melatonin as an adjuvant or standalone cancer treatment.
More Related Videos
Related Concept Videos
02:23Abnormal Proliferation
01:23Negative Regulator Molecules
01:31The Intrinsic Apoptotic Pathway
02:36DNA Damage Can Stall the Cell Cycle
02:36DNA Damage can Stall the Cell Cycle
01:27Molecular Factors Affecting Cell Division
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...