c‐Rel is a transcriptional repressor of <i>EPHB2</i> in colorectal cancer

Fu, Tao; Li, Peng; Wang, Hanzhi; He, Yonghong; Luo, Dong-Hua; Zhang, Anping; Tong, Weidong; Zhang, Lianyang; Liu, Baohua; Hu, Chuanmin

doi:10.1002/path.2590

Cited by 19 publications

(23 citation statements)

References 41 publications

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“…2 In fact, EPHB2 and EPHB3 are transcriptionally inactive in a sizeable fraction of colorectal cancers. [4][5][6][7][8][9] Similar findings exist for EPHB4, 10 and CDX1, another Wnt/β-catenin target important for cellular differentiation and with potential tumor-suppressor functions. [11][12][13][14] However, the molecular mechanisms responsible for downregulation of CDX1 and EPHB2-4 in tumorigenesis despite continuous Wnt/β-catenin pathway activity are a matter of debate.…”

Section: Expression Changes Of Cdx1 and Ephb Receptor Genes In Casemasupporting

confidence: 58%

“…[11][12][13][14] However, the molecular mechanisms responsible for downregulation of CDX1 and EPHB2-4 in tumorigenesis despite continuous Wnt/β-catenin pathway activity are a matter of debate. 7,[15][16][17] One way to achieve transcriptional inactivation of tumor-relevant genes involves alterations of epigenetic features at regulatory regions. 18,19 Hypermethylation of promoter DNA is often found in transformed cells and can silence tumor suppressor genes.…”

Section: Expression Changes Of Cdx1 and Ephb Receptor Genes In Casemamentioning

confidence: 99%

“…3,4,7,16 An association of CDX1 or EphB receptor gene expression with MicrosatelliteInstability (MSI) status or T category, respectively, was not determined because the majority of the investigated carcinomas was MSI negative and T3.…”

Section: O N O T D I S T R I B U T Ementioning

confidence: 99%

See 2 more Smart Citations

Class I and III HDACs and loss of active chromatin features contribute to epigenetic silencing ofCDX1andEPHBtumor suppressor genes in colorectal cancer

Rönsch

Jäger²,

Schöpflin³

et al. 2011

Epigenetics

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Section: Expression Changes Of Cdx1 and Ephb Receptor Genes In Casemasupporting

confidence: 58%

Section: Expression Changes Of Cdx1 and Ephb Receptor Genes In Casemamentioning

confidence: 99%

See 1 more Smart Citation

Class I and III HDACs and loss of active chromatin features contribute to epigenetic silencing ofCDX1andEPHBtumor suppressor genes in colorectal cancer

Rönsch

Jäger²,

Schöpflin³

et al. 2011

Epigenetics

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“…53,54 The downregulation of ephB2 in early and advanced colorectal cancers was found to be due to c-Rel binding to a negative regulatory element in the ephB2 promoter. 52 On the other hand, upregulation of the EphB2 gene is associated with pancreatic ductal adenocarcinoma where it has been shown to be transcriptionally regulated by the Basic transcription factor 3 (BTF3). 55 Another Eph receptor commonly linked to cancer and believed important in tumor metastasis and angiogenesis is ephA2.…”

Section: Misregulationmentioning

confidence: 99%

“…[49][50][51][52] Loss of ephB2 expression is observed in many tumors, and is particularly studied in colonic adenomas and carcinomas. 53,54 The downregulation of ephB2 in early and advanced colorectal cancers was found to be due to c-Rel binding to a negative regulatory element in the ephB2 promoter.…”

Section: Misregulationmentioning

confidence: 99%

Regulation and misregulation of Eph/ephrin expression

Arvanitis¹,

Davy²

2012

Cell Adhesion & Migration

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TNF‐α/TNFR2 Regulatory Axis Stimulates EphB2‐Mediated Neuroregeneration Via Activation of NF‐κB

Pozniak

Darbinyan

Khalili

2015

Journal Cellular Physiology

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HIV-1 infected individuals are at high risk of developing HIV-associated neurocognitive disorders (HAND) as HIV infection leads to neuronal injury and synaptic loss in the central nervous system (CNS). The neurotoxic effects of HIV-1 are primarily a result of viral replication leading to the production of inflammatory chemokines and cytokines, including TNF-alpha. Given an important role of TNF-alpha in regulating synaptic plasticity, we investigated the effects of TNF-alpha on the development of neuronal processes after mechanical injury, and we showed that TNF-alpha treatment stimulates the regrowth of neuronal processes. To investigate transcriptional effects of TNF-alpha on synaptic plasticity, we analyzed both human neurosphere and isolated neuronal cultures for the regulation of genes central to synaptic alterations during learning and memory. TNF-alpha treatment upregulated Ephrin receptor B2 (EphB2), which is strongly involved in dendritic arborization and synaptic integrity. TNF-alpha strongly activates the NF-kappaB pathway, therefore, we propose that TNF-alpha-induced neurite regrowth occurs primarily through EphB2 signaling via stimulation of NF-kappaB. EphB2 promoter activity increased with TNF-alpha treatment and overexpression of NF-kappaB. Direct binding of NF-kappaB to the EphB2 promoter occurred in the ChIP assay, and site-directed mutagenesis identified binding sites involved in TNF-alpha-induced EphB2 activation. TNF-alpha induction of EphB2 was determined to occur specifically through TNF-alpha receptor 2 (TNFR2) activation in human primary fetal neurons. Our observations provide a new avenue for the investigation on the impact of TNF-alpha in the context of HIV-1 neuronal cell damage as well as providing a potential therapeutic target in TNFR2 activation of EphB2.

show abstract

c‐Rel is a transcriptional repressor of EPHB2 in colorectal cancer

Cited by 19 publications

References 41 publications

Class I and III HDACs and loss of active chromatin features contribute to epigenetic silencing ofCDX1andEPHBtumor suppressor genes in colorectal cancer

Class I and III HDACs and loss of active chromatin features contribute to epigenetic silencing ofCDX1andEPHBtumor suppressor genes in colorectal cancer

Regulation and misregulation of Eph/ephrin expression

TNF‐α/TNFR2 Regulatory Axis Stimulates EphB2‐Mediated Neuroregeneration Via Activation of NF‐κB

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