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Loss of expression of LyGDI (ARHGDIB), a rho GDP‐dissociation inhibitor, in Hodgkin lymphoma *
Author(s) -
Ma Liya,
Xu Gaixiang,
Sotnikova Anna,
Szczepanowski Monika,
Giefing Maciej,
Krause Kristina,
Krams Matthias,
Siebert Reiner,
Jin Jie,
Klapper Wolfram
Publication year - 2007
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2007.06782.x
Subject(s) - reed–sternberg cell , apoptosis , cell culture , lymphoma , cancer research , biology , transfection , microbiology and biotechnology , hodgkin lymphoma , immunology , genetics
Summary 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.