TRIB1 overexpression in acute myeloid leukemia

Röthlisberger, Benno; Heizmann, Marc; Bargetzi, Mario; Huber, Andreas

doi:10.1016/j.cancergencyto.2007.03.003

Cited by 34 publications

(31 citation statements)

References 6 publications

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“…Trib1 is elevated in acute myeloid leukemia (AML) and myelodysplastic syndrome patient samples with gene amplifications, and Trib2 is elevated in a subset of AML patient samples. 8,[18][19][20] These findings are supported by murine experiments in which retroviral expression of either Trib1 or Trib2 in BM progenitors caused AML. 8,21 For Trib2, degradation of C/EBP␣ appears to play an important role in the pathogenesis of murine AML.…”

Section: Introductionsupporting

confidence: 72%

Differential ability of Tribbles family members to promote degradation of C/EBPα and induce acute myelogenous leukemia

Dedhia

Keeshan

Uljon

et al. 2010

Blood

141

170

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Trib1, Trib2, and Trib3 are mammalian homologs of Tribbles, an evolutionarily conserved Drosophila protein family that mediates protein degradation. Tribbles proteins function as adapters to recruit E3 ubiquitin ligases and enhance ubiquitylation of the target protein to promote its degradation. Increased Trib1 and Trib2 mRNA expression occurs in human myeloid leukemia and induces acute myeloid leukemia in mice, whereas Trib3 has not been associated with leukemia. Given the high degree of structural conservation among Tribbles family members, we directly compared the 3 mammalian Tribbles in hematopoietic cells by reconstituting mice with hematopoietic stem cells retrovirally expressing these proteins. All mice receiving Trib1 or Trib2 transduced hematopoietic stem cells developed acute myeloid leukemia, whereas Trib3 mice did not. Our previous data indicated that Trib2-mediated degradation of the transcription factor, CCAAT/enhancer-binding protein-alpha (C/EBPα), is important for leukemogenesis. Similar to Trib2, Trib1 induced C/EBPα degradation and inhibited its function. In contrast, Trib3 failed to inactivate or promote efficient degradation of C/EBPα. These data reveal that the 3 Tribbles homologs differ in their ability to promote degradation of C/EBPα, which account for their differential ability to induce leukemia.

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Section: Introductionsupporting

confidence: 72%

Differential ability of Tribbles family members to promote degradation of C/EBPα and induce acute myelogenous leukemia

Dedhia

Keeshan

Uljon

et al. 2010

Blood

141

170

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“…In contrast, constitutive overexpression of trb-1 appears to accelerate the onset of HoxA9/Meis1-induced AML, by enhancing ERK phosphorylation, resulting in inhibition of apoptosis [16]. Moreover, trb-1 has been observed to be overexpressed in AML (two AML/MDS cases [17,18]; an AML case with an additional ring chromosome 8 [19]), and was identified as one of a number of candidate genes thought to be potential targets of genomic amplification in AML with a complex karyotype [20]. Gene expression profiling has identified raised trb-1 expression associated with essential thrombocythaemia (ET), in particular JAK2 V617F-negative ET [21].…”

Section: Introductionmentioning

confidence: 76%

Tribbles-1 and -2 are tumour suppressors, down-regulated in human acute myeloid leukaemia

et al. 2010

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“…7,8 Using the LGA, we analyzed gene expression data from 5 different studies, [9][10][11][12][13] where samples with known AML karyotypes and/or French-American-British (FAB) subtypes were available. Trib1 expression significantly increased in AML with inv(16) or t(16;16) and in FAB M4 and M5 compared with other karyotypes and FAB subtypes (Table 1) and with healthy controls (Table 2).…”

Section: Role Of Tribbles In Acute Myeloid Leukemia (Aml) Trib1mentioning

confidence: 99%

Tribbles in acute leukemia

Liang

Rishi

Keeshan

2013

Blood

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There is growing research interest in the mammalian Tribbles (Trib) family of serine/threonine pseudokinases and their oncogenic association with acute leukemias. This review is to understand the role of Trib genes in hematopoietic malignancies and their potential as targets for novel therapeutic strategies in acute myeloid leukemia and acute lymphoblastic leukemia. We discuss the role of Tribs as central signaling mediators in different subtypes of acute leukemia and propose that inhibition of dysregulated Trib signaling may be therapeutically beneficial.

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TRIB1 overexpression in acute myeloid leukemia

Cited by 34 publications

References 6 publications

Differential ability of Tribbles family members to promote degradation of C/EBPα and induce acute myelogenous leukemia

Differential ability of Tribbles family members to promote degradation of C/EBPα and induce acute myelogenous leukemia

Tribbles-1 and -2 are tumour suppressors, down-regulated in human acute myeloid leukaemia

Tribbles in acute leukemia

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