Transcriptional outcomes and kinetic patterning of gene expression in response to NF-κB activation

Zhao, Mingming; Joy, Jaimy; Zhou, Weiqiang; De, Supriyo; Wood, William H.; Becker, Kevin G.; Ji, Hongkai; Sen, Ranjan

doi:10.1371/journal.pbio.2006347

Cited by 41 publications

(48 citation statements)

References 62 publications

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“…Here, we observed a consistent pattern of cross-activation of the canonical and alternative NF-κB pathways in response to TNF-α and LTβ, the typical ligands for either pathways (43)(44)(45)(46). Although NFKB2 and RELB proteins are the transcription factors subunits of the alternative NF-κB pathway, their gene expression is regulated in part by the classical NF-κB pathway, as they are RELA inducible genes (47). Co-processing of the precursors of NF-κB1 and NF-κB2 proteins has also been linked to bi-directional cross-talk between these pathways (48).…”

Section: Discussionsupporting

confidence: 61%

Head and Neck Cancers Promote an Inflammatory Transcriptome through Coactivation of Classic and Alternative NF-κB Pathways

Yang

Cheng

Chen

et al. 2019

Cancer Immunology Research

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Head and neck squamous cell carcinomas (HNSCC) promote inflammation in the tumor microenvironment through aberrant NF-κB activation, but the genomic alterations and pathway networks that modulate NF-κB signaling have not been fully dissected. Here, we analyzed genome and transcriptome alterations of 279 HNSCC specimens from The Cancer Genome Atlas (TCGA) cohort and identified 61 genes involved in NF-κB and inflammatory pathways. The top 30 altered genes were distributed across 96% of HNSCC samples, and their expression was often correlated with genomic copy number alterations (CNA). Ten of the amplified genes were associated with human papilloma virus (HPV) status. We sequenced 15 HPV(−) and 11 HPV(+) human HNSCC cell lines, and three oral mucosa keratinocyte lines, and supervised clustering revealed that 28/61 genes exhibit altered expression patterns concordant with HNSCC tissues, and distinct signatures related to their HPV status. RNAi screening using an NF-κB reporter line identified 16 genes that are induced by TNF-α or Lymphotoxin β (LTβ) and implicated in the classical and/or alternative NF-κB pathways. Knockdown of TNFR, LTΒR, or selected downstream signaling components established cross-talk between the classical and alternative NF-κB pathways. TNF-α and LTβ induced differential gene expression involving the NF-κB, IFN-γ and STAT pathways, *

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Section: Discussionsupporting

confidence: 61%

Head and Neck Cancers Promote an Inflammatory Transcriptome through Coactivation of Classic and Alternative NF-κB Pathways

Yang

Cheng

Chen

et al. 2019

Cancer Immunology Research

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“…Additionally, overexpression of ANXA2 rescued NF‐κB activation that was inhibited by knockdown S100A11 (Figure E). Moreover, p65 is a classical transcription factor . Next, we determined whether p65 could regulate S100A11 at transcriptional level.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, p65 is a classical transcription factor. 28 Next, we determined whether p65 could regulate S100A11 at transcriptional level. P65 inhibition significantly decreased S100A11 mRNA levels in GBM cells (P < .01, Figure 6F).…”

Section: S100a11 Activates the Nf-κb Pathway By Anxa2 And Nf-κb Rementioning

confidence: 99%

S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop

Xie

et al. 2019

J Cellular Molecular Medi

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Glioblastoma (GBM) is the most universal type of primary brain malignant tumour, and the prognosis of patients with GBM is poor. S100A11 plays an essential role in tumour. However, the role and molecular mechanism of S100A11 in GBM are not clear. Here, we found that S100A11 was up‐regulated in GBM tissues and higher S100A11 expression indicated poor prognosis of GBM patients. Overexpression of S100A11 promoted GBM cell growth, epithelial‐mesenchymal transition (EMT), migration, invasion and generation of glioma stem cells (GSCs), whereas its knockdown inhibited these activities. More importantly, S100A11 interacted with ANXA2 and regulated NF‐κB signalling pathway through decreasing ubiquitination and degradation of ANXA2. Additionally, NF‐κB regulated S100A11 at transcriptional level as a positive feedback. We also demonstrated the S100A11 on tumour growth in GBM using an orthotopic tumour xenografting. These data demonstrate that S100A11/ANXA2/NF‐κB positive feedback loop in GBM cells that promote the progression of GBM.

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“…MZB CKO and eMZB CKO genes were tested for enrichment in NOTCH2 and NF-kB target genes, which were acquired from the Molecular Signatures Database (64) and, in the case of NF-kB target genes, the PageRank analysis from this study and publications involving genetic deletion of NF-kB signaling transcription factors (54,55,(65)(66)(67). NOTCH2 target genes were not significantly enriched in MZB CKO or eMZB CKO (Supplemental Fig.…”

Section: Lsd1 Regulates Ex Vivo Mzb Development Induced By Notch2 Andmentioning

confidence: 99%

LSD1 Cooperates with Noncanonical NF-κB Signaling to Regulate Marginal Zone B Cell Development

Haines

Scharer

Lobby

et al. 2019

The Journal of Immunology

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Transcriptional outcomes and kinetic patterning of gene expression in response to NF-κB activation

Cited by 41 publications

References 62 publications

Head and Neck Cancers Promote an Inflammatory Transcriptome through Coactivation of Classic and Alternative NF-κB Pathways

Head and Neck Cancers Promote an Inflammatory Transcriptome through Coactivation of Classic and Alternative NF-κB Pathways

S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop

LSD1 Cooperates with Noncanonical NF-κB Signaling to Regulate Marginal Zone B Cell Development

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