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Retinoid X receptor suppresses transformation by the v‐ myb oncogene
Author(s) -
Šmarda Jan,
Zemanová Karla,
Bryja Josef,
Šmardová Jana,
Kozubík Alois,
Hofmanová Jirina,
Nemajerová Alice,
Ševçíková Sabina,
Kohoutek Jirí,
Vodiçka Petr
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.66.6.1039
Subject(s) - retinoid x receptor alpha , biology , retinoid x receptor beta , retinoid x receptor gamma , transactivation , retinoid x receptor , retinoic acid , retinoic acid receptor , retinoid , retinoic acid receptor alpha , cancer research , retinoic acid receptor beta , microbiology and biotechnology , cell culture , nuclear receptor , transcription factor , biochemistry , genetics , gene
The v‐ myb oncogene of avian myeloblastosis virus causes acute monoblastic leukemia in vivo and transforms myelomonocytic cells in culture. Retinoids are potent regulators of proliferation and differentiation in various cell types, and they can initiate differentiation in certain types of leukemic cells. However, the BM2 v‐ myb ‐trans‐formed chicken monoblastic cell line is resistant to retinoic acid treatment. We found that overexpression of the retinoid X receptor confers sensitivity of BM2 cells to retinoic acid, resulting in induction of growth arrest and terminal differentiation. In contrast, the frequency of apoptosis was not affected by the retinoid X receptor in this cell type. We also demonstrated that suppression of transformation by v‐Myb results from the negative effect of retinoid X receptor on v‐Myb transactivation function, similar to that previously described for the retinoic acid receptor. The retinoid X receptor‐induced inhibition of transactivation by v‐Myb seems to be enhanced by a cell type‐specific factor(s), which is not required by retinoic acid receptor. J. Leukoc. Biol. 66: 1039–1048; 1999.