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Cadmium modulates H-ras expression and caspase-3 apoptotic cell death in breast cancer epithelial MCF-7 cells

Savvas Petanidis1, Margarita Hadzopoulou-Cladaras, Athanasios Salifoglou

  • 1Laboratory of Inorganic Chemistry, Department of Chemical Engineering, Aristotle University of Thessaloniki, Thessaloniki 54124, Greece.

Journal of Inorganic Biochemistry
|February 5, 2013
PubMed

Insights

Cadmium exposure significantly impacts H-ras oncogene expression and apoptosis in human breast cancer cells. This metal carcinogen affects cell viability and proliferation, revealing interwoven roles in cancer development.

Area of Science:

  • Environmental Toxicology
  • Molecular Carcinogenesis
  • Cell Biology

Background:

  • Cadmium (Cd) is a recognized metal carcinogen linked to tumor formation via mechanisms like DNA repair inhibition, altered gene expression, oxidative stress, and apoptosis.
  • The H-ras oncogene plays a crucial role in carcinogenesis, influencing cellular proliferation and tumorigenesis.

Purpose of the Study:

  • To investigate the concentration-dependent effects of cadmium (Cd(II)) on cell viability, proliferation, caspase-3 mediated apoptosis, and H-ras gene expression.
  • To examine these effects in human breast cancer epithelial MCF-7 cells transfected with wild-type and G12V mutated H-ras oncogenes.

Main Methods:

  • Exposure of MCF-7 cells (transfected with H-ras oncogenes) to varying concentrations of cadmium (Cd(II)).
  • Assessment of cell viability, cell proliferation, caspase-3 activity (apoptosis marker), and H-ras gene expression levels.

Main Results:

  • Cadmium significantly modulated H-ras gene expression in a concentration-dependent manner.
  • An up-regulation of caspase-3 related apoptosis was observed with cadmium exposure (100-1000 nM).
  • A concurrent decrease in MCF-7 cell proliferation was noted.

Conclusions:

  • Cadmium interacts with both wild-type and G12V mutated H-ras, demonstrating concentration-dependent effects on H-ras expression, cell viability, and proliferation.
  • These findings suggest intertwined roles for cadmium and the H-ras oncogene in the aberrant physiology of cancer cells.

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