DIMETHYL-SULFOXIDE (DMSO) CAUSES A REVERSIBLE INHIBITION OF TELOMERASE ACTIVITY IN A BURKITT-LYMPHOMA CELL-LINE

Citation
S. Sharma et al., DIMETHYL-SULFOXIDE (DMSO) CAUSES A REVERSIBLE INHIBITION OF TELOMERASE ACTIVITY IN A BURKITT-LYMPHOMA CELL-LINE, Leukemia research, 22(8), 1998, pp. 663-670
Citations number
31
Categorie Soggetti
Oncology,Hematology
Journal title
ISSN journal
01452126
Volume
22
Issue
8
Year of publication
1998
Pages
663 - 670
Database
ISI
SICI code
0145-2126(1998)22:8<663:D(CARI>2.0.ZU;2-9
Abstract
Introduction: Telomerase is an enzyme that is required for maintenance of telomeres. This enzyme has been shown to be present in germline ti ssues and majority of tumors and tumor cell lines. The regulation of t elomerase is an area of active investigation in different models becau se, potentially, inhibition of this enzyme could be important in cance r therapy. To study the regulation of this enzyme in lymphoma cell lin es, we used DMSO to produce a reversible G0/G1 arrest in Raji cell lin e, as shown earlier [Sawai M, Takase K, Teraoka H, Tsukada K. Reversib le G1 arrest in the cell cycle of human lymphoid cell lines by dimethy l sulphoxide. Exp Cell Res 1990;187:4-10]. Methods: In this study, we use a highly quantifiable conventional (non-amplified) assay to study the effect of DMSO on telomerase. In addition, we studied cellular pro liferation and cell cycle profiles of the cells treated and, subsequen tly, released from DMSO induced blockage. Results: In this model, DMSO reversibly inhibited telomerase activity that could be restored after release from the blockage. The inhibition of telomerase seems to para llel cellular proliferation and it appears that telomerase is regulate d upon entry into the cell cycle. This view is consistent with other p reviously published views on relationship of telomerase with exit from cell cycle. Conclusion. Our observations demonstrate a novel effect o f DMSO on cellular mechanisms in Raji cell line. It may provide an att ractive model to further study regulation of telomerase in this cell l ine. (C) 1998 Elsevier Science Ltd. All rights reserved.