Nicotinamide suppresses cell growth by G1-phase arrest and induces apoptosis in intrahepatic cholangiocarcinoma

被引:4
作者
Wang, Yue [1 ,2 ]
Ryu, Han Suk [1 ]
Jang, Ja June [1 ]
机构
[1] Seoul Natl Univ, Dept Pathol, Coll Med, Seoul, South Korea
[2] Soochow Univ, Dept Human Anat & Histol & Embryol, Sch Biol & Basic Med Sci, Suzhou, Peoples R China
关键词
Apoptosis; Cell Cycle; Cholangiocarcinoma; Invasion; Nicotinamide; EPITHELIAL-MESENCHYMAL TRANSITION; NITRIC-OXIDE PRODUCTION; P53; DEATH; INHIBITION; EXPRESSION; SIRT1; TRIAL; CYCLE; BETA;
D O I
10.1007/s13273-018-0006-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Intrahepatic cholangiocarcinoma (iCCA) is a devastating malignancy with no effective treatment. Nicotinamide (NA, the amide form of vitamin B3) has been shown to be effective in the treatment of various diseases. However, the effects of NA in iCCA have not been studied. In this study, four human iCCA cell lines (HuCCT1, JCK, OZ and Cho-CK) were used. We found that NA significantly inhibited cell viability and induced apoptosis in vitro. It arrested cell cycle in G1 phase, decreased Cyclin D1 and Cdk4 protein expression levels and increased p16 level. NA increased the levels of cleaved caspases 3 and 9, but had no effect on caspase 8. In HuCCT1 and OZ cell lines, NA treatment significantly impaired the invasion abilities and supressed epithelial-mesenchymal transition (EMT)- like changes. In conclusion, our findings provide the experimental basis for using NA as a potential anticancer agent against human iCCA in the future.
引用
收藏
页码:43 / 51
页数:9
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