Department of Biochemistry, Center for Biomedical Mass Spectrometry, Boston University, Boston, Massachusetts, USA.
Department of Biochemistry, Center for Biomedical Mass Spectrometry, Boston University, Boston, Massachusetts, USA; Bioinformatics Program, Boston University, Boston, Massachusetts, USA.
Mol Cell Proteomics. 2022 Apr;21(4):100216. doi: 10.1016/j.mcpro.2022.100216. Epub 2022 Feb 23.
Glioblastoma (GBM) is the most common and malignant primary brain tumor. The extracellular matrix, also known as the matrisome, helps determine glioma invasion, adhesion, and growth. Little attention, however, has been paid to glycosylation of the extracellular matrix components that constitute the majority of glycosylated protein mass and presumed biological properties. To acquire a comprehensive understanding of the biological functions of the matrisome and its components, including proteoglycans (PGs) and glycosaminoglycans (GAGs), in GBM tumorigenesis, and to identify potential biomarker candidates, we studied the alterations of GAGs, including heparan sulfate (HS) and chondroitin sulfate (CS), the core proteins of PGs, and other glycosylated matrisomal proteins in GBM subtypes versus control human brain tissue samples. We scrutinized the proteomics data to acquire in-depth site-specific glycoproteomic profiles of the GBM subtypes that will assist in identifying specific glycosylation changes in GBM. We observed an increase in CS 6-O sulfation and a decrease in HS 6-O sulfation, accompanied by an increase in unsulfated CS and HS disaccharides in GBM versus control samples. Several core matrisome proteins, including PGs (decorin, biglycan, agrin, prolargin, glypican-1, and chondroitin sulfate proteoglycan 4), tenascin, fibronectin, hyaluronan link protein 1 and 2, laminins, and collagens, were differentially regulated in GBM versus controls. Interestingly, a higher degree of collagen hydroxyprolination was also observed for GBM versus controls. Further, two PGs, chondroitin sulfate proteoglycan 4 and agrin, were significantly lower, about 6-fold for isocitrate dehydrogenase-mutant, compared to the WT GBM samples. Differential regulation of O-glycopeptides for PGs, including brevican, neurocan, and versican, was observed for GBM subtypes versus controls. Moreover, an increase in levels of glycosyltransferase and glycosidase enzymes was observed for GBM when compared to control samples. We also report distinct protein, peptide, and glycopeptide features for GBM subtypes comparisons. Taken together, our study informs understanding of the alterations to key matrisomal molecules that occur during GBM development. (Data are available via ProteomeXchange with identifier PXD028931, and the peaks project file is available at Zenodo with DOI 10.5281/zenodo.5911810).
胶质母细胞瘤(GBM)是最常见和最恶性的原发性脑肿瘤。细胞外基质,也称为基质,有助于确定神经胶质瘤的侵袭、黏附和生长。然而,人们对构成糖蛋白大部分质量和假定生物特性的细胞外基质成分的糖基化关注甚少。为了全面了解基质及其成分(包括蛋白聚糖(PGs)和糖胺聚糖(GAGs))在 GBM 肿瘤发生中的生物学功能,并鉴定潜在的生物标志物候选物,我们研究了 GBM 亚型与对照人类脑组织样本中 GAGs(包括肝素硫酸盐(HS)和软骨素硫酸盐(CS))、PG 核心蛋白和其他糖基化基质蛋白的改变。我们仔细研究了蛋白质组学数据,以获得 GBM 亚型的深入、特定于位点的糖蛋白组学图谱,这将有助于鉴定 GBM 中的特定糖基化变化。我们观察到 GBM 与对照样本相比,CS 6-O 硫酸化增加,HS 6-O 硫酸化减少,同时未硫酸化的 CS 和 HS 二糖增加。几种核心基质蛋白,包括蛋白聚糖(decorin、biglycan、agrin、prolargin、glypican-1 和软骨素硫酸盐蛋白聚糖 4)、tenascin、纤连蛋白、透明质酸连接蛋白 1 和 2、层粘连蛋白和胶原,在 GBM 与对照之间存在差异调节。有趣的是,与对照相比,GBM 中的胶原蛋白羟脯氨酸化程度也更高。此外,与 WT GBM 样本相比,两种蛋白聚糖,即软骨素硫酸盐蛋白聚糖 4 和 agrin,在异柠檬酸脱氢酶突变体中显著降低,约为 6 倍。PGs 的 O-糖肽的差异调节,包括 brevican、neurocan 和 versican,在 GBM 亚型与对照之间观察到。此外,与对照样本相比,GBM 中糖基转移酶和糖苷酶酶水平升高。我们还报告了 GBM 亚型比较的独特蛋白质、肽和糖肽特征。综上所述,我们的研究提供了对 GBM 发生过程中关键基质分子变化的理解。(数据可通过 ProteomeXchange 获得,标识符为 PXD028931,峰项目文件可在 Zenodo 上获得,DOI 为 10.5281/zenodo.5911810)。