A DNA-Damage Response Gene Expression Analysis in MCF-7 followed by γ-Radiation

MCF-7 세포주의 γ선에 의한 DNA 손상 반응 유전자 발현 양상의 분석

  • Park Ji-Yoon (Department of Biochem & Mol. Biol, Hanyang University) ;
  • Hwang Chang-Il (Department of Biochem, Seoul National University) ;
  • Park Woong-Yang (Department of Biochem, Seoul National University) ;
  • Kim Jin-Kyu (RI Radiation Research Team, Korea Atomic Energy Research Institute) ;
  • Chai Young Gyu (Department of Biochem & Mol. Biol, Hanyang University)
  • 박지윤 (한양대학교 생화학 및 분자생물학과) ;
  • 황창일 (서울대학교 의과대학 생화학교실) ;
  • 박웅양 (서울대학교 의과대학 생화학교실) ;
  • 김진규 (한국원자력연구소 동위원소 방사선 응용팀) ;
  • 채영규 (한양대학교 생화학 및 분자생물학과)
  • Published : 2005.03.01

Abstract

Cell response to genotoxic agents is complex and involves the participation of different classes of genes including cell cycle control, DNA repair and apoptosis. In this report, we presented a approach to characterize the cellular functions associated with the altered transcript profiles of MCF-7 exposed to low-dose in vitro gamma-irradiation. We used the method of human 2.4 k cDNA microarrays containing apoptosis, cell cycle, chromatin, repair, stress and chromosome genes to analyze the differential gene expression characterization that were displayed by radiation-exposed cell, human breast carcinoma MCF-7 cell line, such as 4 Gy 4 hr, 8 Gy 4 hr, and 8 Gy 12 hr. Among these genes, 66 were up-regulated and 49 were down-regulated. Specific genes were concomitantly induced in the results. Cyclin dependent kinase 4 (Cdk4) is induced for starting the cell cycle. This regulation is required for a DNA damage­induced G1 arrest. In addition to, an apoptotic pathways gene Bcl-w was concomitantly induced. Mismatch repair protein homologue-l (hMLH1), a necessary component of DNA mismatch protein repair (MMR), in G2-M cell cycle checkpoint arrest. The present study provides new information on the molecular mechanism underlying the cell response to genotoxic stress, with relevance to basic and clinical research.

Keywords

References

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