Cytokine-induced cell death in human oligodendroglial cell lines. II: Alterations in gene expression induced by interferon-? and tumor necrosis factor-?

2004 ◽  
Vol 76 (6) ◽  
pp. 846-861 ◽  
Author(s):  
Mieke Buntinx ◽  
Ellen Gielen ◽  
Paul Van Hummelen ◽  
Jef Raus ◽  
Marcel Ameloot ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Cell Lines ◽  
Tumor Necrosis ◽  
Oligodendroglial Cell ◽  
Necrosis Factor

scholarly journals Transcriptional reprogramming and constitutive PD-L1 expression in melanoma are associated with dedifferentiation and activation of interferon and tumor necrosis factor signaling pathways

2021 ◽  
Author(s):  
Antonio Ahn ◽  
Euan J. Rodger ◽  
Gregory Gimenez ◽  
Peter A. Stockwell ◽  
Matthew Parry ◽  
...  
Keyword(s):  
Gene Expression ◽  
Targeted Therapy ◽  
Tumor Necrosis Factor ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Tumor Necrosis ◽  
Melanoma Cells ◽  
Depth Analysis ◽  
Necrosis Factor ◽  
Melanoma Cell Lines

Melanoma is the most aggressive type of skin cancer, with increasing incidence worldwide. Advances in targeted therapy and immunotherapy have improved the survival of melanoma patients experiencing recurrent disease, but unfortunately treatment resistance frequently reduces patient survival. Resistance to targeted therapy is associated with transcriptomic changes, and has also been shown to be accompanied by increased expression of programmed death ligand 1 (PD-L1), a potent inhibitor of immune response. Intrinsic upregulation of PD-L1 is associated with genome-wide DNA hypomethylation and widespread alterations in gene expression in melanoma cell lines. However, an in-depth analysis of the transcriptomic landscape of melanoma cells with intrinsically upregulated PD-L1 expression is lacking. To determine the transcriptomic landscape of intrinsically upregulated PD-L1 expression in melanoma, we investigated tran-scriptomes in melanomas with constitutive versus inducible PD-L1 expression (referred to as PD-L1CON and PD-L1IND). RNA-Seq analysis was performed on seven PD-L1CON melanoma cell lines and ten melanoma cell lines with low inducible PD-L1IND expression. We observed that PD-L1CON melanoma cells had a reprogrammed transcriptome with a characteristic pattern of dedifferentiated gene expression, together with active interferon (IFN) and tumor necrosis factor (TNF) signalling pathways. Furthermore, we identified key transcription factors that were also differentially expressed in PD-L1CON versus PD-L1IND melanoma cell lines. Overall, our studies describe transcriptomic reprogramming of melanomas with PD-L1CON expression.

scholarly journals Involvement of Egr-1/RelA Synergy in Distinguishing T Cell Activation from Tumor Necrosis Factor-α–induced NF-κB1 Transcription

1997 ◽  
Vol 185 (3) ◽  
pp. 491-498 ◽  
Author(s):  
Patricia C. Cogswell ◽  
Marty W. Mayo ◽  
Albert S. Baldwin
Keyword(s):  
Gene Expression ◽  
T Cell ◽  
Tumor Necrosis Factor ◽  
Cell Lines ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Molecular Mechanisms ◽  
T Cell Lines ◽  
Factor Α ◽  
Necrosis Factor

NF-κB is an important transcription factor required for T cell proliferation and other immunological functions. The NF-κB1 gene encodes a 105-kD protein that is the precursor of the p50 component of NF-κB. Previously, we and others have demonstrated that NF-κB regulates the NF-κB1 gene. In this manuscript we have investigated the molecular mechanisms by which T cell lines stimulated with phorbol 12-myristate 13-acetate (PMA) and phytohemagglutin (PHA) display significantly higher levels of NF-κB1 encoding transcripts than cells stimulated with tumor necrosis factor-α, despite the fact that both stimuli activate NF-κB. Characterization of the NF-κB1 promoter identified an Egr-1 site which was found to be essential for both the PMA/ PHA-mediated induction as well as the synergistic activation observed after the expression of the RelA subunit of NF-κB and Egr-1. Furthermore, Egr-1 induction was required for endogenous NF-κB1 gene expression, since PMA/PHA-stimulated T cell lines expressing antisense Egr-1 RNA were inhibited in their ability to upregulate NF-κB1 transcription. Our studies indicate that transcriptional synergy mediated by activation of both Egr-1 and NF-κB may have important ramifications in T cell development by upregulating NF-κB1 gene expression.

RNAi-mediated silencing of insulin receptor substrate-4 enhances actinomycin D- and tumor necrosis factor-α-induced cell death in hepatocarcinoma cancer cell lines

2009 ◽  
Vol 108 (6) ◽  
pp. 1292-1301 ◽  
Author(s):  
Eva P. Cuevas ◽  
Oscar Escribano ◽  
Jorge Monserrat ◽  
Javier Martínez-Botas ◽  
María G. Sánchez ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Insulin Receptor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumor Necrosis ◽  
Actinomycin D ◽  
Insulin Receptor Substrate ◽  
Factor I ◽  
Necrosis Factor
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