Expression of the Gfi-1 gene in HTLV-I-transformed T cells

Citation
I. Sakai et al., Expression of the Gfi-1 gene in HTLV-I-transformed T cells, INT J HEMAT, 73(4), 2001, pp. 507-516
Citations number
42
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Hematology
Journal title
INTERNATIONAL JOURNAL OF HEMATOLOGY
ISSN journal
0925-5710 → ACNP
Volume
73
Issue
4
Year of publication
2001
Pages
507 - 516
Database
ISI
SICI code
0925-5710(200106)73:4<507:EOTGGI>2.0.ZU;2-X
Abstract
Human T-cell leukemia virus type I (HTLV-I) is the causative agent of adult T-cell leukemia/lymphoma (ATLL) and immortalizes human T cells interleukin -2 (IL-2)-dependently in vitro. Protracted culture of HTLV-I-infected T cel ls enables them to grow IL-2-independently. Although acquisition of IL-2-in dependent growth has been correlated with activation of signal transducers and activators of transcription (STATs), the precise mechanism of IL-2-inde pendent growth is unknown. We found that expression of the Gfi-1 (growth factor independence-1) gene w as elevated in most HTLV-I-transformed IL-2-independent cell lines but in f ew HTLV-I-infected IL-2-dependent cell lines. We also found elevated expres sion of Gfi-1 in fresh leukemic cells of ATLL patients. Although expression of Gfi-1 is correlated with activation of STAT3, induction of the dominant negative form of STAT3 in the HUT102 cell line does not alter the level of Gfi-1 expression. Furthermore, MT2 cells treated with Gfi-1 antisense olig onucleotide had reduced [H-3]thymidine uptake compared with MT2 cells treat ed with Gfi-1 sense oligonucleotide, These findings indicate that Gfi-1 act ivation is involved in the IL-2-independent growth of HTLVI-transformed T c ells in vitro and in the development of ATLL in vivo, but is not induced by STAT activation. Int J Hematol. 2001;73:507-516. (C) 2001 The Japanese Soc iety of Hematology.