Related Experiment Video
Updated: Mar 16, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
Low-dose hyper-radiosensitivity in human hepatocellular HepG2 cells is associated with Cdc25C-mediated G2/M cell
Jun Xue1, Yan Zong1, Pin-Dong Li1
1a Cancer Centre, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , China ;
Purpose:
Although the significance of cell cycle checkpoints in overcoming low-dose hyper-radiosensitivity (HRS) has been proposed, the underlying mechanism of HRS in human hepatocellular cells remains unclear. Therefore, the aim of this study was to characterize HRS inhuman hepatocellular HepG2 cells and to explore the molecular mechanism(s) mediating this response.
Materials And Methods:
HepG2 cells were exposed to various single doses of γ radiation (from 0 Gy to 4 Gy), and then were assayed at subsequent time-points. Survival curves were then generated using a linear-quadratic (LQ) equation and a modified induced repair model (MIRM). The percentage of cells in the G1, G2/M, and S phases of the cell cycle were also examined using propidium iodide (PI) staining and flow cytometry. Levels of total cell division cyclin 25C (Cdc25C) and phosphorylated Cdc25C were examined by Western blotting.
Results:
Low-dose γ radiation (<0.3 Gy) induced HRS in HepG2 cells, while doses of 0.3, 0.5, and 2.0 Gy γ radiation significantly arrested HepG2 cells in the G2/M phase. While total Cdc25C levels remained unchanged after irradiation, levels of phosphorylated Cdc25C markedly increased 6, 16, and 24 h after treatment with 0.5 or 2.0 Gy radiation, and they peaked after 16 h. The latter observation is consistent with the G2/M arrest that was detected following irradiation.
Conclusions:
These findings indicate that low-dose HRS in HepG2 cells may be associated with Cdc25C-mediated G2/M cell cycle checkpoint control.
More Related Videos
09:32Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
Published on: October 17, 2025
06:00Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
Published on: May 14, 2016
Related Concept Videos
Inhibition of Cdk Activity
DNA Damage can Stall the Cell Cycle
DNA Damage Can Stall the Cell Cycle
Abnormal Proliferation
Negative Regulator Molecules
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...