NDRG1 and CRK-I/II are regulators of endothelial cell migration under intermittent hypoxia

Toffoli, Sébastien; Delaive, Edouard; Dieu, Marc; Feron, Olivier; Raes, Martine; Michiels, Carine

doi:10.1007/s10456-009-9156-2

Cited by 26 publications

(20 citation statements)

References 40 publications

(55 reference statements)

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“…There were some reports claiming the opposite. Some studies indicated that the upregulation of NDRG1 was observed in various tumors where it would increase cancer cell metastasis [30,32]. Our results showed its expression did not associate with lymph node, so the controversial role of its expression in cancer metastasis needs more further research to confirm.…”

Section: Discussioncontrasting

confidence: 59%

Increased N-myc downstream-regulated gene 1 expression is associated with breast atypia-to-carcinoma progression

et al. 2011

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N-myc downstream-regulated gene-1 (NDRG1) has been identified as a protein involved in the differentiation of epithelial cells. As a newly metastasis suppressor gene, whether it contributes to carcinogenesis of breast cancer is still unknown. This study aimed to clarify the possible role of NDRG1 for breast cancer carcinogenesis, and further to investigate its clinicopathological significance in invasive breast cancer. We examined the expression of NDRG1 in normal epithelium of breast (n = 35), usual ductal hyperplasia (n = 22), atypical ductal hyperplasia (n = 33), atypical lobular hyperplasia (n = 8), ductal carcinoma in situ (n = 16), lobular carcinoma in situ (n = 6), invasive ductal carcinoma (n = 50), and invasive lobular carcinoma (n = 45) by immunohistochemistry and analyzed the correlation between NDRG expression and clinicopathological features of invasive breast cancer. Western blot analysis was carried out to investigate the expression of NDRG1 in 20 invasive ductal breast cancer and the paired non-tumor portion of the same case. NDRG1 expression in invasive breast cancer (70/95, 73.7%) was higher than that in noninvasive breast lesions (29/85, 34.1%; p < 0.05) which was higher than that in normal breast epithelium (5/35, 14.3%; p < 0.05). Statistical analysis revealed a significant correlation between NDRG1 expression with tumor stage in invasive breast cancer, and its expression in invasive ductal carcinoma is significantly higher than invasive lobular carcinoma (p < 0.05). It was not associated with age, menopausal status, tumor size, and lymph node metastasis. NDRG1 protein levels were significantly higher in invasive ductal breast cancer compared to the paired non-tumor portion of the same case by Western blot analysis (p < 0.05). Increased NDRG-1 expression is associated with breast atypia-to-carcinoma progression. NDRG1 expression might participate in the carcinogenesis and progression of invasive breast cancer. These findings provide further evidence that NDRG1 may serve as an important biomarker for invasive breast cancer.

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Section: Discussioncontrasting

confidence: 59%

Increased N-myc downstream-regulated gene 1 expression is associated with breast atypia-to-carcinoma progression

et al. 2011

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“…DUSP5, NRARP) regulate angiogenesis ( Fig. 9H) (Al-Greene et al, 2013;Bellou et al, 2009;Herbert et al, 2012;Iaccarino et al, 2005;Mirza et al, 2013;Moehler et al, 2008;Phng et al, 2009;Pin et al, 2012;Prahst et al, 2014;Toffoli et al, 2009;Zhou et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Dynamic regulation of VEGF-inducible genes by an ERK-ERG-p300 transcriptional network

et al. 2017

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The transcriptional pathways activated downstream of vascular endothelial growth factor (VEGF) signaling during angiogenesis remain incompletely characterized. By assessing the signals responsible for induction of the Notch ligand delta-like 4 (DLL4) in endothelial cells, we find that activation of the MAPK/ERK pathway mirrors the rapid and dynamic induction of DLL4 transcription and that this pathway is required for DLL4 expression. Furthermore, VEGF/ERK signaling induces phosphorylation and activation of the ETS transcription factor ERG, a prerequisite for DLL4 induction. Transcription of DLL4 coincides with dynamic ERG-dependent recruitment of the transcriptional co-activator p300. Genome-wide gene expression profiling identified a network of VEGF-responsive and ERG-dependent genes, and ERG chromatin immunoprecipitation (ChIP)-seq revealed the presence of conserved ERG-bound putative enhancer elements near these target genes. Functional experiments performed in vitro and in vivo confirm that this network of genes requires ERK, ERG and p300 activity. Finally, genome-editing and transgenic approaches demonstrate that a highly conserved ERG-bound enhancer located upstream of HLX (which encodes a transcription factor implicated in sprouting angiogenesis) is required for its VEGFmediated induction. Collectively, these findings elucidate a novel transcriptional pathway contributing to VEGF-dependent angiogenesis.

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“…NDRG1 and CrkI/II are indeed regulators of endothelial cell migration under IH: silencing of CrkI/II resulted in an increase in endothelial cell migration, whereas the invalidation of NDRG1 decreased it. 53 …”

Section: Crk In Endothelial Cellsmentioning

confidence: 99%

Roles for Crk in Cancer Metastasis and Invasion

Tsuda¹,

Tanaka

2012

Genes & Cancer

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The Crk family of adaptors is implicated in regulating various biological and pathological processes such as cell proliferation, adhesion, migration, invasion, phagocytosis, and survival. A large number of studies have shown that Crk plays an important role in aggressive and malignant behaviors of human cancers. In immunohistochemical analyses and gene-expression profiles, enhanced expression of Crk has been identified in adenocarcinomas of lung, breast, and stomach and in sarcomas and glioma. Overexpression of Crk in tumor cells induces the prominent tyrosine phosphorylations of scaffolding molecules such as p130Cas and paxillin through Src family tyrosine kinases and stimulates the activation loop of intracellular signalling, ultimately contributing to the increased motility and aggressive potential of cancer cells. Crk proteins thus are not simply conduits for intracellular signal transduction but also can control the amplitude of signalling. This review summarizes the significance of Crk and its mediated signaling assemblies, particularly in regulating tumor metastasis and invasion, and discusses the possibilities that they are potential cancer therapeutic targets.

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NDRG1 and CRK-I/II are regulators of endothelial cell migration under intermittent hypoxia

Cited by 26 publications

References 40 publications

Increased N-myc downstream-regulated gene 1 expression is associated with breast atypia-to-carcinoma progression

Increased N-myc downstream-regulated gene 1 expression is associated with breast atypia-to-carcinoma progression

Dynamic regulation of VEGF-inducible genes by an ERK-ERG-p300 transcriptional network

Roles for Crk in Cancer Metastasis and Invasion

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