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논문 기본 정보
- 자료유형
- 학위논문
- 저자정보
- 발행연도
- 2018
- 저작권
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Doxorubicin is a general chemotherapy drug widely used for a number of cancers. However, the correlation between endogenous nitric oxide (NO?) levels and chemoresistance to Doxorubicin remains unclear. In this study we investigated the effect of endogenous NO? on the anticancer activity of Doxorubicin in human colon cancer cell lines HCT116 and HT29 with different p53 status. Cells were treated with either Doxorubicin alone or in combination with NO? synthase (NOS) inhibitor NG-monomethyl-L-arginine (NMA). We show that Doxorubicin differentially inhibits the growth of both HCT116 (p53-WT) and HT29 (p53-MUT) cells, which was mitigated by cotreatment with NMA. Further studies reveal that inhibition of endogenous
NO? mitigates Doxorubicin-induced apoptosis in HCT116 and HT29 cells as evidenced by apoptotic DNA fragmentation and sub-G1 peak of apoptotic markers detection: Apoptosis was delayed and greatly reduced in magnitude in HT29 cells, underscoring the importance of p53 modulation of the response. RT-PCR analysis revealed that Doxorubicin down-regulated levels of inhibitors of apoptosis family (cellular IAP-1 and -2). Collectively, these data show that induction of apoptosis by Doxorubicin in human colon cancer cells
is possibly related with modulation of endogenous NO?, IAP family geneexpression and p53 status. The underlying mechanisms may thus represent potential targets for adjuvant strategies to improve the efficacy of
chemotherapy for colon cancer.
NO? mitigates Doxorubicin-induced apoptosis in HCT116 and HT29 cells as evidenced by apoptotic DNA fragmentation and sub-G1 peak of apoptotic markers detection: Apoptosis was delayed and greatly reduced in magnitude in HT29 cells, underscoring the importance of p53 modulation of the response. RT-PCR analysis revealed that Doxorubicin down-regulated levels of inhibitors of apoptosis family (cellular IAP-1 and -2). Collectively, these data show that induction of apoptosis by Doxorubicin in human colon cancer cells
is possibly related with modulation of endogenous NO?, IAP family geneexpression and p53 status. The underlying mechanisms may thus represent potential targets for adjuvant strategies to improve the efficacy of
chemotherapy for colon cancer.
목차
Contents ⅰList of Tables ⅲList of Figures ⅳAbstract ⅴⅠ. 서 론 1Ⅱ. 재료 및 방법1. 실험재료 72. 세포배양 73. Trypan blue assay에 의한 세포 생존율 측정 74. Griess assay에 의한 산화질소 생성량 측정 85. Reverse transcription polymerase chain reacion에 의한 산화질소 합성효소 (Nitric oxide synthase)의 mRNA 발현 분석 86. Flow cytometry에 의한 세포주기 분석 97. Doxorubicin 처리에 의한 DNA 단편화 측정 98. 통계분석 10Ⅲ. 결 과 111. Doxorubicin과 NMA 병용 처리에 의한 대장암 세포의 생존율 변화 112. Doxorubicin과 NMA 병용 처리에 의한 산화질소 생성량 변화 133. 대장암 세포에서 Doxorubicin에 의한 NOS 발현 변화 154. 대장암 세포에서 Doxorubicin에 의한 세포주기 변화 175. 대장암 세포에서 Doxorubicin에 의한 Apoptosis 유발 196. 대장암 세포에서 Doxorubicin에 의한 Inhibitor of apoptosis protein (IAP)발현 변화 21Ⅳ. 고 찰 23Ⅴ. 참 고 문 헌 26Ⅵ. 요 약 30
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