Department of Chemistry, University of California Davis, Davis, CA 95616, USA.
Mol Cell Proteomics. 2011 Jan;10(1):M110.002717. doi: 10.1074/mcp.M110.002717. Epub 2010 Nov 19.
Alteration in glycosylation has been observed in cancer. However, monitoring glycosylation changes during breast cancer progression is difficult in humans. In this study, we used a well-characterized transplantable breast tumor mouse model, the mouse mammary tumor virus-polyoma middle T antigen, to observe early changes in glycosylation. We have previously used the said mouse model to look at O-linked glycosylation changes with breast cancer. In this glycan biomarker discovery study, we examined N-linked glycan variations during breast cancer progression of the mouse model but this time doubling the number of mice and blood draw points. N-glycans from total mouse serum glycoproteins were profiled using matrix-assisted laser desorption/ionization Fourier transform-ion cyclotron resonance mass spectrometry at the onset, progression, and removal of mammary tumors. We observed four N-linked glycans, m/z 1339.480 (Hex(3)HexNAc), 1485.530 (Hex(3)HexNAc(4)Fuc), 1809.639 (Hex(5)HexNAc(4)Fuc), and 1905.630 (Man(9)), change in intensity in the cancer group but not in the control group. In a separate study, N-glycans from total human serum glycoproteins of breast cancer patients and controls were also profiled. Analysis of human sera using an internal standard showed the alteration of the low-abundant high-mannose glycans, m/z 1419.475, 1581.528, 1743.581, 1905.634 (Man(6-9)), in breast cancer patients. A key observation was the elevation of a high-mannose type glycan containing nine mannoses, Man(9), m/z 1905.630 in both mouse and human sera in the presence of breast cancer, suggesting an incompletion of the glycosylation process that normally trims back Man(9) to produce complex and hybrid type oligosaccharides.
糖基化的改变在癌症中已经被观察到。然而,在人类中监测乳腺癌进展过程中的糖基化变化是困难的。在这项研究中,我们使用了一种经过良好表征的可移植乳腺癌肿瘤小鼠模型,即鼠乳腺肿瘤病毒-多瘤病毒中 T 抗原,来观察糖基化的早期变化。我们之前使用所述的小鼠模型来观察乳腺癌中的 O 连接糖基化变化。在这项聚糖生物标志物发现研究中,我们检查了小鼠模型中乳腺癌进展过程中的 N 连接聚糖变化,但这次将小鼠数量和采血点加倍。使用基质辅助激光解吸/电离傅里叶变换离子回旋共振质谱法,在乳腺肿瘤的起始、进展和消除时,对来自总小鼠血清糖蛋白的 N-聚糖进行了分析。我们观察到四个 N-连接聚糖,m/z 1339.480(Hex(3)HexNAc)、1485.530(Hex(3)HexNAc(4)Fuc)、1809.639(Hex(5)HexNAc(4)Fuc)和 1905.630(Man(9)),在癌症组中强度发生变化,但在对照组中没有。在另一项研究中,还对乳腺癌患者和对照组的总人血清糖蛋白中的 N-聚糖进行了分析。使用内部标准对人血清进行分析表明,低丰度高甘露糖聚糖,m/z 1419.475、1581.528、1743.581、1905.634(Man(6-9)),在乳腺癌患者中的改变。一个关键的观察结果是,在存在乳腺癌的情况下,来自小鼠和人血清的高甘露糖型聚糖升高,m/z 1905.630,含有九个甘露糖,表明糖基化过程不完全,该过程通常将 Man(9)修剪回产生复杂和混合型寡糖。