Liu A-J, Song W, Yang N, Liu Y-J, Zhang G-R
Tianjin Key Laboratory of Food Nutrition and Safety, Institute of Food Engineering and Biotechnology, Tianjin University of Science and Technology, Tianjin, PR China.
Cell Biol Toxicol. 2007 Nov;23(6):465-76. doi: 10.1007/s10565-007-9008-z. Epub 2007 May 22.
In this study, we extracted a polysaccharide (short-chain polysaccharide [PS]) from porcine cartilage and examined its function in chronic myeloid leukaemia by using human K562 cells and mouse L1210 cells. Results of cell proliferation assay indicated that PS inhibited cancer cell growth at different concentrations, while it had little effect on normal cells. The presence of morphological aspects of apoptosis, such as nuclear shrinkage, was shown in H&E stained sections. The occurrence of PS-induced apoptosis was confirmed by TUNEL assay and cell cycle analysis. The results of immunofluorescent staining indicated the molecular mechanism underlying. Through interfering with the cell cycle of tumor cells, PS may induce apoptosis by downregulating the expression level of cyclin D1 and upregulating the level of p21 protein. Correlation analysis of apoptosis and MAPK suggested that inactivation of ERK was crucial for PS induced apoptosis, while JNK phosphorylation had a small effect and p38 was not involved. In vivo assay showed that PS inhibited L1210 cell growth in vivo and prolonged the life span of L1210-bearing mice. We conclude that PS is a polysaccharide with anticancer effects and induced apoptosis in human K562 cells.
在本研究中,我们从猪软骨中提取了一种多糖(短链多糖[PS]),并使用人K562细胞和小鼠L1210细胞研究了其在慢性髓性白血病中的作用。细胞增殖试验结果表明,PS在不同浓度下均能抑制癌细胞生长,而对正常细胞影响较小。苏木精-伊红(H&E)染色切片显示存在凋亡的形态学特征,如核固缩。TUNEL检测和细胞周期分析证实了PS诱导凋亡的发生。免疫荧光染色结果表明了其潜在的分子机制。通过干扰肿瘤细胞的细胞周期,PS可能通过下调细胞周期蛋白D1的表达水平和上调p21蛋白水平来诱导凋亡。凋亡与丝裂原活化蛋白激酶(MAPK)的相关性分析表明,细胞外信号调节激酶(ERK)失活对PS诱导的凋亡至关重要,而c-Jun氨基末端激酶(JNK)磷酸化作用较小,p38不参与其中。体内试验表明,PS在体内抑制L1210细胞生长,并延长了荷L1210小鼠的生存期。我们得出结论,PS是一种具有抗癌作用的多糖,可诱导人K562细胞凋亡。