NF-kB in development and progression of human cancer

Dolcet, Xavier; Llobet, David; Pallarés, Judit; Matías‐Guiu, Xavier

doi:10.1007/s00428-005-1264-9

Cited by 1,022 publications

(862 citation statements)

References 71 publications

(63 reference statements)

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“…T-cell neoplasms (Gilmore et al, 1996;Dolcet et al, 2005). In Jurkat cells, LYL1 interacts with NF-kB1 p105, a precursor of NF-kB, and inhibits NF-kBdependent transcription by reducing NF-kB activity (Ferrier et al, 1999).…”

Section: Lyl1 Overexpression Causes T-and B-cell Lymphoma Y Zhong Et Almentioning

confidence: 99%

Overexpression of a transcription factor LYL1 induces T- and B-cell lymphoma in mice

et al. 2007

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LYL1, a member of the class II basic helix-loop-helix transcription factors, is aberrantly expressed in a fraction of human T-cell acute lymphoblastic leukemia. Here, we generated transgenic mice ubiquitously overexpressing LYL1 using a construct expressing full-length cDNA driven by a human elongation factor 1a promoter. Four independent lines exhibiting high LYL1 expression were established. Of these transgenic mice, 96% displayed loss of hair with a short kinked tail. Furthermore, 30% of them developed malignant lymphoma, with an average latent period of 352 days. In these mice, histological examination revealed tumor cell infiltration in multiple organs and immunohistochemical analysis showed that the infiltrated tumor cells were either CD3 or CD45R/B220-positive; fluorescence-activated cell sorter analysis indicated that each tumor consisted either of mainly CD4, CD8 double-positive T cells or mature B cells; the clonality of LYL1-induced lymphoma was confirmed by T-cell receptor rearrangement and immunoglobulin heavychain gene rearrangement analyses. Mammalian twohybrid analysis and luciferase assay suggested that excess LYL1 blocked the dimerization of E2A and thus inhibited the regulatory activity of E2A on the CD4 promoter. Reverse transcription-polymerase chain reaction results showed that the expression of certain E2A/HEB target genes was downregulated. Taken together, our results provide direct evidence that aberrant expression of LYL1 plays a role in lymphomagenesis.

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Section: Lyl1 Overexpression Causes T-and B-cell Lymphoma Y Zhong Et Almentioning

confidence: 99%

Overexpression of a transcription factor LYL1 induces T- and B-cell lymphoma in mice

et al. 2007

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“…This phosphorylation leads to its poly-ubiquitinylation and subsequent proteasomal degradation (Zandi et al, 1997). NF-KB over-expression is seen in the progression of several cancers, including multiple myeloma (Dolcet et al, 2005). NF-KB blocks TNF-oinduced apoptosis by activation of c-FLIP either directly or through inhibition of JNK (Russo et al, 2001).…”

Section: Trail: Other Signaling Pathwaysmentioning

confidence: 99%

Modulation of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptors in a human osteoclast model in vitro

et al. 2011

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“…Furthermore, menin has been reported to interact with NF-kB proteins and to inhibit the NF-kB-mediated transcriptional activation (Heppner et al, 2001). An NF-kB activation has been reported in several human neoplasias including breast cancers, prostate tumors, melanoma, hepatocellular carcinomas and pancreatic cancer (Dolcet et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Relation between menin expression and NF-κB activity in an intestinal cell line

Theillaumas

Blanc

Couderc

et al. 2008

Molecular and Cellular Endocrinology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t AbstractIn a previous study, we demonstrated that the Men1 gene is mainly expressed in the proliferative crypt compartment of the small intestine and that a reduction of menin expression in the crypt-like IEC-17 cell line induces an increase in proliferation rate concomitant with an increase in cyclin D1 expression. The aim of the present study was to test the hypothesis that the NF-kB pathway may be involved in cyclin D1 overexpression.Transcriptional activity of the cyclin D1 gene promoter was increased upon reduction of menin expression. Blockade of the NF-kB pathway restored proliferation, cell cycle, cyclin D1 gene transcription and cyclin D1 expression levels to those observed in the presence of menin. These data support a correlation between cyclin D1 expression, NF-kB activity and menin expression in this epithelial cell line and are relevant to the physiological function of menin in regulating proliferation in the intestinal epithelium.

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NF-kB in development and progression of human cancer

Cited by 1,022 publications

References 71 publications

Overexpression of a transcription factor LYL1 induces T- and B-cell lymphoma in mice

Overexpression of a transcription factor LYL1 induces T- and B-cell lymphoma in mice

Modulation of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptors in a human osteoclast model in vitro

Relation between menin expression and NF-κB activity in an intestinal cell line

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