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정상세포와 암세포의 증식 억제에 대한 에탄올의 영향

Anti-Proliferative Effect of Ethanol on Normal and Cancer Cells

  • 오명주 (식품의약청 임상시험관리부) ;
  • 김지현 (부산대학교 나노과학기술대학 나노메디컬공학과) ;
  • 박수현 (부산대학교 나노과학기술대학 나노메디컬공학과) ;
  • 정영화 (부산대학교 나노과학기술대학 나노메디컬공학과) ;
  • 왕쿤 (부산대학교 생명자원과학대학 동물자원학과) ;
  • 조병욱 (부산대학교 생명자원과학대학 동물자원학과) ;
  • 전병학 (부산대학교 나노과학기술대학 나노메디컬공학과)
  • Oh, Myung-Ju (Division of Clinical Trials Management, Bureau of Risk Prevention Policy, Korea Food and Drug Administration) ;
  • Kim, Ji-Hyun (Department of Nanomedical Engineering, Pusan National University) ;
  • Park, Su-Hyun (Department of Nanomedical Engineering, Pusan National University) ;
  • Jeong, Young-Hwa (Department of Nanomedical Engineering, Pusan National University) ;
  • Wang, Kun (Department of Animal Sciences, Pusan National University) ;
  • Cho, Byung-Wook (Department of Animal Sciences, Pusan National University) ;
  • Jhun, Byung-H. (Department of Nanomedical Engineering, Pusan National University)
  • 투고 : 2012.02.17
  • 심사 : 2012.03.22
  • 발행 : 2012.04.30

초록

에탄올은 사람에 대한 발암물질로 잘 알려져 있다. 또한 여러 조직이나 세포에서의 에탄올에 의한 세포증식억제효과도 잘 알려져 있다. 본 연구에서는 여러 암세포에서 에탄올에 의한 세포증식억제 효과를 조사하였는데 특히 발암원성 $ras$로 형질전환되거나 미세주입된 세포에서의 영향을 조사하였다. 에탄올은 여러 정상세포들의 증식을 억제하였다. 반면에 여러 암세포나 발암원성 Ras에 의한 세포증식은 억제하지 못 하였다. 또한 발암원성 단백질의 세포내 미세주사에 의한 DNA합성 유도도 에탄올에 의해 억제 되지 않았다. 이러한 에탄올의 세포증식억제 효과는 $N$-acetylcysteine이나 4-methylpyrazole과 같은 항산화제에 의해 제거되었다. 이러한 실험 결과는 에탄올에 의한 세포증식억제 효과는 Ras단백질의 upstream에 있거나 또는 Ras와 독립적으로 작용하며, 활성산소 형성과 밀접한 관계가 있다는 것을 알려준다.

Ethanol is known as being carcinogenic to humans. In addition, the anti-proliferative effects of ethanol have been described for a variety of tissues and cells. In this study, we investigated the anti-proliferative effects of ethanol on various cancer cells, particularly on oncogenic $ras$-transformed or-injected cells. Ethanol treatment inhibited the cell proliferation of normal control cells, but did not suppress the proliferation of various cancer cells and oncogenic $ras$-transformed cells. Furthermore, ethanol treatment did not interfere with DNA synthesis, which was induced by microinjecting the oncogenic $H-Ras^{V12}$ protein. The anti-proliferative effect of ethanol was rescued by antioxidants, such as $N$-acetylcysteine and 4-methlpyrazole. These results suggest that ethanol cytotoxicity is exerted through free radical formation, and that the anti-proliferative action site of ethanol cytotoxicity either lies upstream, or is independent of Ras.

키워드

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