Oncotarget

Research Papers:

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

Alexandra Y. Tsidulko _, Liudmila Matskova, Lidiia A. Astakhova, Ingemar Ernberg and Elvira V. Grigorieva

PDF  |  HTML  |  Supplementary Files  |  How to cite  |  Order a Reprint

Oncotarget. 2015; 6:43529-43539. https://doi.org/10.18632/oncotarget.5984

Metrics: PDF 754 views  |   HTML 1118 views  |   ?  


Abstract

Alexandra Y. Tsidulko1,2, Liudmila Matskova2, Lidiia A. Astakhova3, Ingemar Ernberg2, Elvira V. Grigorieva1,2

1Institute of Molecular Biology and Biophysics, Novosibirsk, Russia

2Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institute, Stockholm, Sweden

3Kemerovo Institute of Food Science and Technology, Kemerovo, Russia

Correspondence to:

Elvira V. Grigorieva, e-mail: elv_grig@yahoo.com

Keywords: Epstein-Barr virus, B cells, lymphoma development, proteoglycan, heparan sulfate biosynthesis

Received: August 21, 2015     Accepted: October 06, 2015     Published: October 16, 2015

ABSTRACT

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.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 5984