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Superoxide dismutase induces G1-phase cell cycle arrest by down-regulated expression of Cdk-2 and cyclin-E in murine

Dongyue Liu1, Anjun Liu

  • 1Tianjin University of Science and Technology, Key Laboratory of Food Nutrition and Safety, Ministry of Education, Institute of Food Engineering and Biotechnology, Tianjin, China.

Cell Biochemistry and Function
|October 12, 2012
PubMed

Insights

Superoxide dismutase (SOD) effectively halts the proliferation of S180 tumor cells by inducing cell cycle arrest at the G1-phase. This mechanism involves reducing superoxide levels and down-regulating key proteins like cyclin-E and Cdk-2.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Superoxide dismutase (SOD) is a reactive oxygen species-scavenging enzyme with demonstrated anti-tumor properties.
  • SOD can inhibit cancer cell growth, motility, and invasiveness.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying SOD-induced cell cycle arrest in S180 tumor cells.
  • To determine the optimal conditions for SOD treatment in S180 cells.

Main Methods:

  • Murine sarcoma S180 tumor cells and NIH-3T3 mouse fibroblasts were treated with varying concentrations of Cu/Zn-SOD for 24, 48, and 72 hours.
  • Cell cycle progression, superoxide production, Proliferating Cell Nuclear Antigen (PCNA) expression, and levels of cyclin-E and Cdk-2 were analyzed.

Main Results:

  • The optimal dose of SOD was determined to be 800 U/ml for 48 hours.
  • SOD induced G1-phase cell cycle arrest in S180 cells, accompanied by decreased superoxide production.
  • SOD treatment suppressed PCNA expression and down-regulated cyclin-E and Cdk-2 in S180 cells, inhibiting DNA synthesis and G1/S transition.
  • SOD exhibited minimal effects on NIH-3T3 cell proliferation.

Conclusions:

  • SOD effectively inhibits S180 tumor cell proliferation by inducing G1-phase cell cycle arrest.
  • The mechanism involves the down-regulation of cyclin-E and Cdk-2, leading to the blockage of G1/S transition.
  • SOD demonstrates selective anti-proliferative effects on tumor cells compared to normal fibroblasts.

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