Effect of chitooligosaccharides on cyclin D1, bcl-xl and bcl-2 mRNA expression in A549 cells using quantitative PCR

被引:20
|
作者
Li Xian [1 ]
Wang Ju [2 ]
Chen XiaoJia [2 ]
Tian JinHuan [1 ]
Li LiHua [1 ]
Zhao MingYan [1 ]
Jiao YanPeng [1 ]
Zhou ChangRen [1 ]
机构
[1] Jinan Univ, Dept Mat Sci & Engn, Guangzhou 510632, Guangdong, Peoples R China
[2] Jinan Univ, Bioengn Inst, Guangzhou 510632, Guangdong, Peoples R China
来源
CHINESE SCIENCE BULLETIN | 2011年 / 56卷 / 15期
基金
国家高技术研究发展计划(863计划);
关键词
chitooligosaccharides; cyclin D1; bcl-xl; bcl-2; FAMILY-MEMBERS; CANCER; APOPTOSIS; OLIGOSACCHARIDES; DRIVER; COS;
D O I
10.1007/s11434-010-4501-9
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Chitooligosaccharide (COS) is derived from the chemical and enzymatic hydrolysis of chitosan and has been reported to have potent antitumor activity. Our study investigated the effects of five chitooligomers ranging from the dimer form to the hexamer form (chitobiose, chitotriose, chitotetraose, chitopentaose, chitohexaose) on the expression of cyclin D1, bcl-2 and bcl-xl mRNA in A549 cells using reverse transcription quantitative real-time PCR. We demonstrated that, of the five chitooligomers used, chitohexaose (COS6) had the most potent inhibitory effect on A549 cell proliferation. COS6 also significantly down regulated cyclin D1 and bcl-xl mRNA expression levels. Our data suggested that COS6 exerts its antitumor activity by two different mechanisms: (1) COS6-mediated inhibition of Cyclin D1 levels leads to suppression of tumor cell proliferation; and (2) COS6-mediated down-regulation of the pro-survival protein, Bcl-xl, promotes the apoptosis of tumor cells.
引用
收藏
页码:1629 / 1632
页数:4
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