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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2006.1
- 수록면
- 54 - 60 (7page)
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초록· 키워드
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Purpose: Treatment with arsenic trioxide (As2O3) results in a wide range of cellular effects that includes induction of apoptosis, inhibition of cell growth, promotion or inhibition of cellular differentiation, and inhibition of angiogenesis through a variety of mechanisms. The mechanisms of As2O3-induced cell death have been mainly studied in hematological cancers, and those mechanisms in solid cancers have yet to be clearly defined. In this study, the mechanisms by which As2O3 induces apoptosis in human colorectal adenocarcinoma HT-29 cells were investigated.
Materials and Methods: To examine the levels of apoptosis, HT-29 cells were treated with As2O3 and then we measured the percentage of Annexin V binding cells, the amount of ROS production and the mitochondrial membrane potential. Western blot analysis was performed to identify the activated caspases after As2O3 exposure, and we compared the possible target molecules of apoptosis. As2O3 treatment induced the loss of the mitochondrial membrane potential and an increase of ROS, as well as activation of caspase-3, -7, -9 and -10.
Results: As2O3 induced apoptosis via the production of reactive oxygen species and the loss of the mitochondrial membrane potential. As2O3 induced the activation of caspase-3, -7, -9 and -10. Furthermore, As2O3 treatment downregulates the Mcl-1 and Bcl-2 expressions, and the release of cytochrome c and an apoptosis-inducing factor (AIF). Pretreating the HT-29 cells with N-acetyl-L-cysteine, which is a thiol-containing antioxidant, inhibited the As2O3- induced apoptosis and caspase activation.
Conclusion: Taken together, these results suggest that the generation of reactive oxygen species (ROS) by As2O3 might play an important role in the regulation of As2O3- induced apoptosis. This cytotoxicity is mediated through a mitochondria-dependent apoptotic signal pathway in HT-29 cells. (Cancer Res Treat. 2006;38:54-60)
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참고문헌 (24)
참고문헌 신청
/ / United States multicenter study of arsenic trioxide in relapsed acute promyelocytic leukemia 19 : 3852 ~ 3860
/ 1996 / Bcl-2 inhibits the mitochondrial release of an apoptogenic protease 184 : 1331 ~ 1341
/ 1997 / Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade 91 : 479 ~ 489
/ 1997 / JC-1, but not DiOC6 (3) or rhodamine 123, is a reliable fluorescent probe to assess delta psi changes in intact cells 411 : 77 ~ 82
/ 1998 / The Bcl-2 protein family: arbiters of cell survival 281 : 1322 ~ 1626
/ 1996 / Bcl-2 inhibits the mitochondrial release of an apoptogenic protease 184 : 1331 ~ 1341
/ 1997 / Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade 91 : 479 ~ 489
/ 1997 / JC-1, but not DiOC6 (3) or rhodamine 123, is a reliable fluorescent probe to assess delta psi changes in intact cells 411 : 77 ~ 82
/ 1998 / The Bcl-2 protein family: arbiters of cell survival 281 : 1322 ~ 1626
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