CAJ | 학술논문

[目的]通过实验研究观察千金藤素（Cepharanthine，CEP）对人结肠癌的抗增殖作用。[方法]本研究通过活体荧光示踪技术研究CEP对人结肠癌细胞HCT116裸鼠异体移植肿瘤模型的抗结肠癌作用，运用报告基因技术研究CEP对肿瘤相关的8条信号通路活化程度的影响，采用流式细胞仪测定CEP对细胞周期分布的影响。[结果]CEP体外能抑制多种人源肿瘤细胞的增殖，IC50范围为0.8-11.5μM。CEP能使HCT116细胞的S期和G2/M期百分比明显增加。通过对MAPK/ERK、MAPK/JNK、Wnt、Notch、Cel Cycle/pRb-E2F、NFκB、Myc/Max以及Hypoxia等8条信号通路报告基因活化程度的研究，发现CEP主要通过抑制MAPK/ERK和NFκB信号通路起到抑制肿瘤增殖的作用。动物模型的实验结果显示，CEP能抑制肿瘤增殖，促进肿瘤组织坏死。[结论]CEP通过抑制MAPK/ERK和NFκB信号通路的活化抑制人结肠癌细胞HCT116裸鼠异体移植肿瘤的增殖。
[목적]통과실험연구관찰천금등소（Cepharanthine，CEP）대인결장암적항증식작용。[방법]본연구통과활체형광시종기술연구CEP대인결장암세포HCT116라서이체이식종류모형적항결장암작용，운용보고기인기술연구CEP대종류상관적8조신호통로활화정도적영향，채용류식세포의측정CEP대세포주기분포적영향。[결과]CEP체외능억제다충인원종류세포적증식，IC50범위위0.8-11.5μM。CEP능사HCT116세포적S기화G2/M기백분비명현증가。통과대MAPK/ERK、MAPK/JNK、Wnt、Notch、Cel Cycle/pRb-E2F、NFκB、Myc/Max이급Hypoxia등8조신호통로보고기인활화정도적연구，발현CEP주요통과억제MAPK/ERK화NFκB신호통로기도억제종류증식적작용。동물모형적실험결과현시，CEP능억제종류증식，촉진종류조직배사。[결론]CEP통과억제MAPK/ERK화NFκB신호통로적활화억제인결장암세포HCT116라서이체이식종류적증식。
[Objective]To investigate the anti-proliferative effects of CEP on HCT116 cells and in mouse xenograft model. [Methods]The in vivo anti-cancer activity of CEP was determined with Xenogen bioluminescence imaging in a xenograft tumor model. The cel-based multiple signaling pathway reporter assays were carried out to determine the effects of CEP on these pathways. [Results] CEP inhibited growth of human cancer cells, the IC 50 was 0.8~11.5 μM. CEP induced cellcycle arrest in S and G2/M phase. CEP also inhibited xenograft tumor growth in athymic nude mice bearing HCT116 cells. The xenograft tumor size was significantly reduced upon the treatment with CEP(10 or 20 mg·kg-1 body weight) for up to 3 weeks. Pathway-spe-cific reporter assays indicated that CEP effectively suppressed the NF-κB and MAPK/ERK signaling pathways. [Conclusions] Our results suggest that the anticancer activity of CEP in colon cancer cells may be mediated through targeting NF-κB and MAPK/ERK signaling pathways.