Oncoprotein v-Myb and Retinoic Acid Receptor α Are Mutual Antagonists

Zemanová, Karla; Šmarda, Jan

doi:10.1006/bcmd.1998.0189

Cited by 9 publications

(12 citation statements)

References 33 publications

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“…The hypothesis that c-Fos functions as a transcriptional repressor in order to activate programmed cell death is further supported by the fact that the protein synthesis inhibitor CHX did not block c-Fos-induced apoptosis of BM2cFOS cells. v-Myb shares proliferation-promoting and apoptosissuppressing activities with c-Myb but it does not permit the activation of genes required for terminal differentiation of its cellular progenitor [57,70,71]. This study and our previous paper [27] document that transcription factors Fos and Jun that form the AP-1 complex can significantly affect the function of the v-Myb oncoprotein.…”

Section: Discussionmentioning

confidence: 55%

c-Fos but not v-Fos protein induces programmed cell death of v-myb-transformed monoblasts

Zahradníčková

Souček

Ševčı́ková

et al. 2003

CMLS, Cell. Mol. Life Sci.

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c-Fos and v-Fos belong to a group of proteins forming the transcription factor AP-1 that is important for regulation of proliferation, differentiation and programmed cell death in multiple cell types. In this study, we examined the role of c-Fos and v-Fos proteins in v-myb-transformed BM2 monoblasts. We show that while the v-Fos protein prolongs the G0G1 phase of the BM2 cell cycle, c-Fos leaves the cell cycle unaffected and, rather, induces programmed cell death. The apoptosis-promoting activity of the c-Fos protein is markedly enhanced in cells cultivated under serum-free conditions. c-Fos-induced apoptosis of BM2 cells occurred in the presence of Bcl-2 and was not dependent on the transcription activation function of the c-Fos protein. No differentiation-promoting activity of the Fos proteins was observed. The effects of Fos proteins on BM2 cells differ from those induced by Jun proteins, suggesting differential roles of individual components of the AP-1 transcription factor in regulation of essential cellular processes.

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Section: Discussionmentioning

confidence: 55%

c-Fos but not v-Fos protein induces programmed cell death of v-myb-transformed monoblasts

Zahradníčková

Souček

Ševčı́ková

et al. 2003

CMLS, Cell. Mol. Life Sci.

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“…We and others recently described that the v-Myb and RAR proteins reciprocally modify each others' functions, thus they can be considered as mutual antagonists [41][42][43]69]. RAR␣ expressed in v-myb-transformed monoblasts suppressed transformation and permitted RA-dependent differentiation into macrophage-like cells [41].…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, the v-myb-transformed monoblasts expressing either RAR␣ or RXR␣ differentiate without apoptosis on activation by RA. The number of apoptotic cells detected in a population of RA-treated BM2RAR␣ and BM2RXR␣ cells was very low, suggesting that there is an efficient block of apoptotic processes in BM2 cells, presumably resulting from anti-apoptotic activities of v-Myb oncoprotein [42,58,59]. In contrast, treatment of BM2 cells with TPA induces both differentiation and apoptosis [50].…”

Section: Discussionmentioning

confidence: 99%

“…The conditions for cultivation and transient transfection of BM2 cells were described elsewhere [42,50]. In brief, 5 µg of the reporter plasmid (Ew5LUC or TK-CRBPII-LUC) and 5 µg of an internal control cmv-␤gal plasmid were mixed with 5 ϫ 10 6 of exponentially growing BM2, BM2RAR␣, and BM2RXR␣ cells in 400 µL of standard cultivation medium, including sera containing 1.25% dimethyl sulfoxide (DMSO).…”

Section: Cell Cultivation and Transfectionmentioning

confidence: 99%

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Retinoid X receptor suppresses transformation by the v-myb oncogene

Šmarda

Zemanová

Bryja

et al. 1999

Journal of Leukocyte Biology

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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-transformed 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.

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“…In addition, BM2 cells treated with TPA or expressing p53 share other features: they exit cell cycle in the G2-phase and differentiate to mostly mononuclear derivatives (Sˇmarda and Lipsick, 1994;Nemajerova et al, 2003). In contrast, the G1-phase blockers and differentiation inducers, such as trichostatin A or retinoic acid suppress transactivation by the v-Myb oncoprotein and increase formation of multinuclear macrophage-like cells (Sˇmarda et al, 1995;Zemanova and Sˇmarda, 1998;Vodicka et al, 2000;Nemajerova et al, 2003;Sˇmardova´et al, 2005). The G1-phase cell cycle arrest and formation of multinucleated giant cells also occur in chicken yolk sac cells transformed with v-Myb-estrogen receptor fusion protein and withdrawn from estrogen (Engelke et al, 1997).…”

Section: Activity Of the V-myb Oncoprotein Increases In P53-expressinmentioning

confidence: 99%