Deregulation of common genes by c-Myc and its direct target, MT-MC1

Rogulski, Kenneth; Cohen, Daniel J.; Corcoran, David L.; Benos, Panayiotis V.; Prochownik, Edward V.

doi:10.1073/pnas.0507902102

Cited by 24 publications

(38 citation statements)

References 46 publications

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“…As shown in Figure 6a, GpIba was detected in all cases, with the highest levels occurring in cancer lines. Consistent with our previous report (Rogulski et al, 2005b), a notable correlation between c-Myc and GpIba expression was seen (Figure 6b). Finally, a search of the Oncomine database (http://www.oncomine.org; Rhodes et al, 2004) indicated that GpIba transcripts were overexpressed in germ cell tumors vs normal testicular tissue (P ¼ 0.001; Korkola et al, 2006), in imatinibresistant chronic myelogenous leukemia vs untreated chronic-phase disease (P ¼ 7 Â 10 À7 ; Radich et al, 2006;Figure 6c), and in c-src-transformed primary human mammary epithelial cells (Bild et al, 2006).…”

Section: Increased Expression Of Gpiba In Cancersupporting

confidence: 93%

“…One such target, MT-MC1, encodes a nuclear protein with the unique ability to reproduce multiple c-Myc functions (Yin et al, 2002;Rothermund et al, 2005). Surprisingly, MT-MC1 deregulates o50 genes most of which are also direct c-Myc targets (Rogulski et al, 2005b). These findings suggest that MT-MC1-regulated genes comprise a 'privileged' subset of c-Myc targets with a disproportionate role in mediating c-Myc phenotypes.…”

mentioning

confidence: 97%

“…Despite this molecular complexity, a number of c-Myc target genes are themselves transforming and/or able to recapitulate other c-Myc phenotypes (reviewed in Rogulski et al, 2005b). One such target, MT-MC1, encodes a nuclear protein with the unique ability to reproduce multiple c-Myc functions (Yin et al, 2002;Rothermund et al, 2005).…”

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confidence: 99%

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Transformation, genomic instability and senescence mediated by platelet/megakaryocyte glycoprotein Ibα

Cohen

et al. 2007

Oncogene

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GpIba, a subunit of the von Willebrand factor receptor, functions during blood clotting to promote platelet adhesion and activation. GpIba is widely expressed, is positively regulated by c-Myc and is essential for the promotion of c-Myc-mediated chromosomal instability. We now show that GpIba is also a classical oncoprotein in which its deregulated expression leads to transformation, reduced growth factor requirements, increased resistance to apoptosis, and, in primary cells, p53-dependent senescence. Finally, GpIba also promotes double-stranded DNA breaks, and induces profound nuclear dysmorphology, indicating that, in addition to its direct transforming function, it displays genotoxicity at several distinct levels. These findings identify novel functions for GpIba and pathways through which c-Myc mediates transformation and global genomic destabilization.

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Section: Increased Expression Of Gpiba In Cancersupporting

confidence: 93%

mentioning

confidence: 97%

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Transformation, genomic instability and senescence mediated by platelet/megakaryocyte glycoprotein Ibα

Cohen

et al. 2007

Oncogene

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“…Rogulski et al . identified 47 genes deregulated by MT‐MC1 using transcriptional profiling 11. However, they did not find DNA binding domain in MT‐MC1 protein or consensus DNA binding sequences.…”

Section: Introductionmentioning

confidence: 95%

Transmembrane domain is crucial to the subcellular localization and function of Myc target 1

Gui

Yin

et al. 2015

J Cellular Molecular Medi

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Deregulation of c‐MYC occurs in a variety of human cancers. Overexpression of c‐MYC promotes cell growth, proliferation, apoptosis, transformation and genomic instability. MYC target 1 (MYCT1) is a direct target gene of c‐MYC, and its murine homologue MT‐MC1 recapitulated multiple c‐Myc‐related phenotypes. However, the molecular mechanism of MYCT1 remains unclear. Here, we identified the transmembrane (TM) domain of MYCT1, not the nuclear localization sequence, is indispensable to the vesicle‐associated localization of MYCT1 protein in the cytoplasmic membrane vesicle. Overexpression of MYCT1, not MYCT1 (ΔTM), decreased cell viability under serum deprivation and increased tumour cell migration ability. We further identified CKAP4 interacted with MYCT1 and contributed to the function of MYCT1. In addition, we found that a mutation, A88D, which is observed in patient sample, changed the localization, and abolished the effect on cell viability and cell migration, suggesting that the TM domain is critical to MYCT1.

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“…56,57 In order to gain insight into the molecular basis for MT-MC1's unique properties, we conducted a DNA microarray study to identify its target genes in myeloid cells. 58 In contrast to the mind-numbing myriad of c-Myc targets, only 47 genes were de-regulated by MT-MC1. Furthermore, all twelve genes from this group that we examined were also found to be independent targets of c-Myc.…”

Section: An Unexpected Role For a Megakaryocytic Endomitosis Pathway mentioning

confidence: 99%

The Ever Expanding Role for c-Myc in Promoting Genomic Instability

Prochownik¹,

Li²

2007

Cell Cycle

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Deregulation of common genes by c-Myc and its direct target, MT-MC1

Cited by 24 publications

References 46 publications

Transformation, genomic instability and senescence mediated by platelet/megakaryocyte glycoprotein Ibα

Transformation, genomic instability and senescence mediated by platelet/megakaryocyte glycoprotein Ibα

Transmembrane domain is crucial to the subcellular localization and function of Myc target 1

The Ever Expanding Role for c-Myc in Promoting Genomic Instability

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