Loss of expression of LyGDI (ARHGDIB), a rho GDP-dissociation inhibitor, in Hodgkin lymphoma

被引:40
作者
Ma, Liya
Xu, Gaixiang
Sotnikova, Anna
Szczepanowski, Monika
Giefing, Maciej
Krause, Kristina
Krams, Matthias
Siebert, Reiner
Jin, Jie
Klapper, Wolfram
机构
[1] Schleswig Holstein Univ Hosp, Dept Pathol Haematopathol, D-24105 Kiel, Germany
[2] Schleswig Holstein Univ Hosp, Lymph Node Registry, D-24105 Kiel, Germany
[3] Zhejiang Univ, Affiliated Hosp 1, Dept Haematol, Hangzhou 310027, Peoples R China
[4] Schleswig Holstein Univ Hosp, Inst Human Genet, Kiel, Germany
[5] Polish Acad Sci, Inst Human Genet, PL-60479 Poznan, Poland
关键词
Hodgkin lymphoma; LyGDI; apoptosis; ARHGDIB;
D O I
10.1111/j.1365-2141.2007.06782.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The guanosine triphosphatase (GTPase) inhibitor LyGDI (ARHGDIB, Ly/D4-GDI, RhoGDIb or RhoGDI 2) is abundantly expressed in haematopoetic cells and possibly plays a role in the onset of apoptosis. Gene expression profiling of Hodgkin cell lines revealed that LyGDI expression was downregulated in these cell lines. The present study evaluated the expression of LyGDI in Hodgkin cells in vivo and studied the function of LyGDI in Hodgkin cell lines in vitro. Our results showed that virtually all Hodgkin and Reed-Sternberg cells in classical Hodgkin lymphoma lacked LyGDI protein expression. On the other hand, almost all non-Hodgkin lymphomas, except for anaplastic large cell lymphomas, expressed LyGDI protein. Transfection of the classical Hodgkin cell line L428 with a vector containing full-length LyGDI-induced apoptosis in a subset of cells. However, the majority of Hodgkin cells with transgenic expression of LyGDI escaped apoptosis. Our data show that lack of LyGDI expression is a frequent feature of cHL but that it is not of vital importance for the growth and survival of these cells.
引用
收藏
页码:217 / 223
页数:7
相关论文
共 18 条
  • [1] IMMUNOENZYMATIC LABELING OF MONOCLONAL-ANTIBODIES USING IMMUNE-COMPLEXES OF ALKALINE-PHOSPHATASE AND MONOCLONAL ANTI-ALKALINE PHOSPHATASE (APAAP COMPLEXES)
    CORDELL, JL
    FALINI, B
    ERBER, WN
    GHOSH, AK
    ABDULAZIZ, Z
    MACDONALD, S
    PULFORD, KAF
    STEIN, H
    MASON, DY
    [J]. JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1984, 32 (02) : 219 - 229
  • [2] RhoGDI: Multiple functions in the regulation of Rho family GTPase activities
    Dovas, A
    Couchman, JR
    [J]. BIOCHEMICAL JOURNAL, 2005, 390 : 1 - 9
  • [3] Expression of the cellular FLICE-inhibitory protein (c-FLIP) protects Hodgkin's lymphoma cells from autonomous Fas-mediated death
    Dutton, A
    O'Neil, JD
    Milner, AE
    Reynolds, GM
    Starczynski, J
    Crocker, J
    Young, LS
    Murray, PG
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (17) : 6611 - 6616
  • [4] GDP dissociation inhibitor D4-GDI (Rho-GDI 2), but not the homologous Rho-GDI 1, is cleaved by caspase-3 during drug-induced apoptosis
    Essmann, F
    Wieder, T
    Otto, A
    Müller, EC
    Dörken, B
    Daniel, PT
    [J]. BIOCHEMICAL JOURNAL, 2000, 346 (pt 3) : 777 - 783
  • [5] Heidebrecht HJ, 1997, BLOOD, V90, P226
  • [6] Jaffe ES., 2001, PATHOLOGY GENETICS T
  • [7] Hodgkin and Reed-Sternberg cells in Hodgkin's disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells
    Kanzler, H
    Kuppers, R
    Hansmann, ML
    Rajewsky, K
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 184 (04) : 1495 - 1505
  • [8] DNA damage transiently increases TRF2 mRNA expression and telomerase activity
    Klapper, W
    Qian, W
    Schulte, C
    Parwaresch, R
    [J]. LEUKEMIA, 2003, 17 (10) : 2007 - 2015
  • [9] Küppers R, 1999, NEW ENGL J MED, V341, P1520
  • [10] Identification of Hodgkin and Reed-Sternberg cell-specific genes by gene expression profiling
    Küppers, R
    Klein, U
    Schwering, I
    Distler, V
    Bräuninger, A
    Cattoretti, G
    Tu, Y
    Stolovitzky, GA
    Califano, A
    Hansmann, ML
    Dalla-Favera, R
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (04) : 529 - 537