Nuclear cytokine-activated IKKalpha controls prostate cancer metastasis by repressing Maspin (Q28294196)

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Wei Tan

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Jill M Ricono

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Olexandr Korchynskyi

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Ming Zhang

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Steven L Gonias

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David A Cheresh

NF-kappaB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression

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language of work or name

English

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publication date

5 April 2007

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published in

Nature

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volume

446

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page(s)

690-4

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issue

7136

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cites work

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IKKalpha provides an essential link between RANK signaling and cyclin D1 expression during mammary gland development

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Prostate cancer in a transgenic mouse

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Maspin, a serpin with tumor-suppressing activity in human mammary epithelial cells

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Pathological and molecular aspects of prostate cancer

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Prostate carcinoma I: prognostic factors in radical prostatectomy specimens and pelvic lymph nodes

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The IKK NF-kappa B system: a treasure trove for drug development

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A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB

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Pathobiology of autochthonous prostate cancer in a pre‐clinical transgenic mouse model

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Metastasis suppressors alter the signal transduction of cancer cells

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Maspin plays an important role in mammary gland development

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Reduced mammary tumor progression in WAP-TAg/WAP-maspin bitransgenic mice

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Maspin expression inhibits osteolysis, tumor growth, and angiogenesis in a model of prostate cancer bone metastasis

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Tumor suppressive maspin and epithelial homeostasis

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Activation by IKKalpha of a second, evolutionary conserved, NF-kappa B signaling pathway

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Potentiation of neuroblastoma metastasis by loss of caspase-8.

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p53 regulates the expression of the tumor suppressor gene maspin

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IkappaB kinase-alpha acts in the epidermis to control skeletal and craniofacial morphogenesis

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Activation of IKKalpha target genes depends on recognition of specific kappaB binding sites by RelB:p52 dimers

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I{kappa}B kinase (IKK){beta}, but not IKK{alpha}, is a critical mediator of osteoclast survival and is required for inflammation-induced bone loss

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Smoldering and polarized inflammation in the initiation and promotion of malignant disease

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Maspin and tumor metastasis

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Identification of maspin and S100P as novel hypomethylation targets in pancreatic cancer using global gene expression profiling

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Methyltransferase recruitment and DNA hypermethylation of target promoters by an oncogenic transcription factor

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Regulation of cancer cell migration and bone metastasis by RANKL.

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Inhibition of NF-kappaB in cancer cells converts inflammation- induced tumor growth mediated by TNFalpha to TRAIL-mediated tumor regression

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Mouse colon carcinoma cells established for high incidence of experimental hepatic metastasis exhibit accelerated and anchorage-independent growth.

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Identifiers

DOI

10.1038/NATURE05656

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Consolidated OpenCitations Corpus – April 2017

Dimensions Publication ID

1456322

1027634754

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1456322

1 reference

Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference