c-Myc is essential for vasculogenesis and angiogenesis during development and tumor progression

Baudino, Troy A.; McKay, Catriona; Pendeville-Samain, Hélène; Nilsson, Jonas A.; Maclean, Kirsteen H.; White, Elsie; Davis, A C; Ihle, James N.; Cleveland, John L.

doi:10.1101/gad.1024602

Cited by 443 publications

(413 citation statements)

References 51 publications

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“…Interference with hypoxia-responsive differentiation may be widely involved in leukemia initiation and progression. For example, it is postulated that CMYC and HIF1 share common target genes (Dang and Semenza, 1999) and VEGF was recently presented as an indirect CMYC target gene (Baudino et al, 2002). Whether CMYC and hypoxia common target genes play a role in leukemogenesis remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Functional analyses of the TEL-ARNT fusion protein underscores a role for oxygen tension in hematopoietic cellular differentiation

et al. 2006

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The transcription factor hypoxia inducible factor 1 (HIF1), an HIF1a-aryl hydrocarbon receptor nuclear translocator (ARNT) dimeric factor, is essential to the cellular response to hypoxia. We described a t(1;12)(q21;p13) chromosomal translocation in human acute myeloblastic leukemia that involves the translocated Ets leukemia (TEL/ETV6) and the ARNT genes and results in the expression of a TEL-ARNT fusion protein.Functional studies show that TEL-ARNT interacts with HIF1a and the complex binds to consensus hypoxia response element. In low oxygen tension conditions, the HIF1a/TEL-ARNT complex does not activate transcription but exerts a dominant-negative effect on normal HIF1 activity. Differentiation of normal human CD34 þ progenitors cells along all the erythrocytic, megakaryocytic and granulocytic pathways was accelerated in low versus high oxygen tension conditions. Murine 32Dcl3 myeloid cells also show accelerated granulocytic differentiation in low oxygen tension in response to granulocyte colony-stimulating factor. Interestingly, stable expression of the TEL-ARNT in 32Dcl3 subclones resulted in impaired HIF1-mediated transcriptional response and inhibition of differentiation enhancement in hypoxic conditions. Taken together, our results underscore the role of oxygen tension in the modulation of normal hematopoietic differentiation, whose targeting can participate in human malignancies.

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Section: Discussionmentioning

confidence: 99%

Functional analyses of the TEL-ARNT fusion protein underscores a role for oxygen tension in hematopoietic cellular differentiation

et al. 2006

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“…29 MYC has a crucial role in growth control, differentiation and apoptosis, and its aberrant expression is associated with several cancers. More recently, MYC was also implicated as having a major contribution in tumor angiogenesis, 33,34 by upregulating one of its direct targets, the miR-17-92 cluster. The predicted targets of miR-17-92 cluster are thrombospondin-1 (THBS1), encoding a potent endogenous inhibitor of angiogenesis, and connective tissue growth factor (CTGF), encoding an extracellular matrix-associated molecule involved in angiogenesis and metastatic progression.…”

Section: Geneticsmentioning

confidence: 99%

Malignant vascular tumors—an update

2014

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“…In addition, numerous studies showed that Myc activation was sufficient to provoke diverse cancers (Adams et al, 1985;Leder et al, 1986) and, more recently, that Myc is continuously required to maintain the transformed state (Felsher and Bishop, 1999;Pelengaris et al, 1999;Jain et al, 2002). Finally, to round out the story was the revelation that c-Myc functioned as an angiogenic switch (Pelengaris et al, 1999(Pelengaris et al, , 2002, and that its expression was in fact essential for proper and coordinate regulation of angiogenic and anti-angiogenic factors in cancer and development (Baudino et al, 2002). This was satisfying -now we know why Myc activation was so pervasive in cancer.…”

Section: The Myc Paradoxmentioning

confidence: 99%