Related Experiment Video

Updated: Aug 22, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Modifications in cell cycle kinetics and in expression of G1 phase-regulating proteins in human amniotic cells after

S Lange1, T Viergutz, M Simkó

  • 1Research Centre Rossendorf, Institute of Bioinorganic and Radiopharmaceutical Chemistry, Dresden, Germany.

Cell Proliferation
|September 21, 2004
PubMed

Insights

Low-frequency electromagnetic fields (MF) did not alter cell cycle kinetics in human cells. However, MF exposure alone decreased cyclin D1 and increased p21CIP1 and p16INK4a expression, without affecting mutagenic potential with ionizing radiation.

Area of Science:

  • Cell Biology
  • Biophysics
  • Cancer Research

Background:

  • Low-frequency electromagnetic fields (MF) are implicated in carcinogenesis, potentially promoting cancer via deregulated cell growth.
  • Previous research indicated MF exposure can decrease DNA synthesis.
  • Understanding MF effects on cell cycle regulation is crucial for assessing cancer risk.

Purpose of the Study:

  • To investigate the impact of 50 Hz, 1 mT MF exposure, with or without gamma-ionizing radiation (IR), on cell proliferation parameters in human amniotic fluid cells (AFC).
  • To analyze changes in cell cycle distribution, G1 regulatory protein expression (Cdk4, cyclin D1, p21CIP1, p16INK4a), and Cdk4 activity.

Main Methods:

  • Human amniotic fluid cells (AFC) were exposed to 50 Hz, 1 mT MF, with or without prior gamma-ionizing radiation (IR).
  • Cell cycle distribution was analyzed.
  • Protein levels of Cdk4, cyclin D1, p21CIP1, and p16INK4a were quantified via Western blotting.
  • Cdk4 kinase activity was measured.

Main Results:

  • Ionizing radiation (IR) induced a G1 delay and G2 arrest, while MF exposure alone did not alter cell cycle kinetics.
  • MF exposure significantly decreased cyclin D1 protein expression and increased p21CIP1 and p16INK4a expression.
  • IR increased p21CIP1 and p16INK4a but did not affect cyclin D1.
  • A slight decrease in Cdk4 activity was observed after MF exposure only.
  • Combined MF/IR exposure showed no synergistic effects on cell cycle, protein expression, or kinase activity.

Conclusions:

  • MF exposure alone alters cell cycle regulatory proteins (cyclin D1, p21CIP1, p16INK4a) but does not affect cell cycle progression or Cdk4 activity significantly in AFCs.
  • MF does not appear to modify the mutagenic potential of ionizing radiation in this cellular model.
  • Cdk4 may not be the primary mediator of MF- or IR-induced cellular changes.

More Related Videos

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress09:51

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress

Published on: May 7, 2014

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry08:21

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry

Published on: September 1, 2019

Related Concept Videos

DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Nondisjunction01:21

Nondisjunction

Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold sister...
Molecular Factors Affecting Cell Division01:27

Molecular Factors Affecting Cell Division

Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit 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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...