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Cyclin A expression is associated with apoptosis and mitosis in murine 3-methylcholanthrene-induced fibrosarcomas

M Sozmen1, R Tunca, S Dag Erginsoy

  • 1Department of Pathology, University of Kafkas, Pasacayiri, Kars, Turkey. msozmen@hotmail.com

Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Fur Toxikologische Pathologie
|July 16, 2008
PubMed

Insights

Methylcholanthrene (MCA) induced fibrosarcomas in mice, revealing low expression of iNOS and Cu/Zn-SOD. Cyclin A was highly expressed and correlated with apoptosis, suggesting its role in fibrosarcoma development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Reactive oxygen species (ROS) are crucial in cancer development, but their expression patterns in methylcholanthrene (MCA)-induced fibrosarcomas are not well understood.
  • Inducible nitric oxide synthase (iNOS) and copper/zinc superoxide dismutase (Cu/Zn-SOD) are key players in cellular redox balance and cancer progression.
  • Cyclin A, a cell cycle regulator, is frequently overexpressed in tumors, yet its specific role in MCA-induced fibrosarcomas, particularly concerning mitosis and apoptosis, remains unclear.

Purpose of the Study:

  • To investigate the expression patterns of iNOS and Cu/Zn-SOD in MCA-induced fibrosarcomas.
  • To analyze the expression of Cyclin A in relation to mitotic activity and apoptosis in these tumors.
  • To elucidate the potential role of Cyclin A in the pathogenesis of MCA-induced fibrosarcomas.

Main Methods:

  • Immunohistochemical analysis was used to assess the expression of iNOS, Cu/Zn-SOD, and Cyclin A in fibrosarcoma tissues.
  • The TUNEL assay was employed to evaluate the incidence of apoptotic cell death.
  • Mitotic counts were performed and correlated with Cyclin A expression and TUNEL-positive reactions.

Main Results:

  • MCA induced fibrosarcoma development in 70% of mice within 26 weeks.
  • Limited cytoplasmic expression of Cu/Zn-SOD and iNOS was observed in the majority of tumors.
  • All fibrosarcoma cases exhibited prominent nuclear Cyclin A immunostaining and TUNEL-positive reactions, with Cyclin A expression significantly correlating with both the TUNEL index and mitotic count.

Conclusions:

  • The low expression of iNOS suggests limited synthesizing capacity in MCA-induced fibrosarcoma cells.
  • Limited Cu/Zn-SOD expression may indicate an imbalance in the pro-oxidant/antioxidant levels within the tumors.
  • Overexpression of Cyclin A in MCA-induced fibrosarcomas suggests its significant role in tumor pathogenesis, potentially by inducing S-phase arrest associated with apoptosis.

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