Proteoglycan expression correlates with the phenotype of malignant and non-malignant EBV-positive B-cell lines

• Published in: Oncotarget 2015-12, Vol.6 (41), p.43529-43539
• Main Authors: Tsidulko, Alexandra Y, Matskova, Liudmila, Astakhova, Lidiia A, Ernberg, Ingemar, Grigorieva, Elvira V
• Format: Article
• Language: English
• Subjects: B-Lymphocytes - metabolism; B-Lymphocytes - virology; Blotting, Western; Burkitt Lymphoma - metabolism; Burkitt Lymphoma - virology; Cell Line, Tumor; Cell Transformation, Neoplastic - metabolism; Epstein-Barr Virus Infections - metabolism; Flow Cytometry; Herpesvirus 4, Human - physiology; Humans; Medicin och hälsovetenskap; Phenotype; Proteoglycans - biosynthesis; Real-Time Polymerase Chain Reaction; Research Paper; Virus Latency
• ISSN: 1949-2553; 1949-2553
• DOI: 10.18632/oncotarget.5984

The involvement of proteoglycans (PGs) in EBV-host interactions and lymphomagenesis remains poorly investigated. In this study, expression of major proteoglycans (syndecan-1, glypican-1, perlecan, versican, brevican, aggrecan, NG2, serglycin, decorin, biglycan, lumican, CD44), heparan sulphate (HS) metabolic system (EXT1/2, NDST1/2, GLCE, HS2ST1, HS3ST1/2, HS6ST1/2, SULF1/2, HPSE) and extracellular matrix (ECM) components (collagen 1A1, fibronectin, elastin) in primary B cells and EBV carrying cell lines with different phenotypes, patterns of EBV-host cell interaction and viral latency stages (type I-III) was investigated. Primary B cells expressed a wide repertoire of PGs (dominated by serglycin and CD44) and ECM components. Lymphoblastoid EBV+ B cell lines (LCLs) showed specific PG expression with down-regulation of CD44 and ECM components and up-regulation of serglycin and perlecan/HSPG2. For Burkitt's lymphoma cells (BL), serglycin was down-regulated in BL type III cells and perlecan in type I BL cells. The biosynthetic machinery for HS was active in all cell lines, with some tendency to be down-regulated in BL cells. 5'-aza-dC and/or Trichostatin A resulted in transcriptional upregulation of the genes, suggesting that low expression of ECM components, proteoglycan core proteins and HS biosynthetic system is due to epigenetic suppression in type I cells. Taken together, our data show that proteoglycans are expressed in primary B lymphocytes whereas they are not or only partly expressed in EBV-carrying cell lines, depending on their latency type program.