ArticleOncogene2005
Immortalized fibroblasts from NF-kappaB RelA knockout mice show phenotypic heterogeneity and maintain increased sensitivity to tumor necrosis factor alpha after transformation by v-Ras.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Natural Compound Dioscin Targeting Multiple Cancer Pathways through its High Affinity Binding to B Cell Lymphoma-2.Current computer-aided drug design · 2025Article
- The NF-κB multidimer system model: A knowledge base to explore diverse biological contexts.Science signaling · 2023Review
- TAK1 signaling regulates p53 through a mechanism involving ribosomal stress.Scientific reports · 2020Article
- Quercetin inhibits prostate cancer by attenuating cell survival and inhibiting anti-apoptotic pathways.World journal of surgical oncology · 2018Article
- NF-κB, the Importance of Being Dynamic: Role and Insights in Cancer.Biomedicines · 2018Review
- Regulation of SET Gene Expression by NFkB.Molecular neurobiology · 2017Article
- MEK and TAK1 Regulate Apoptosis in Colon Cancer Cells with KRAS-Dependent Activation of Proinflammatory Signaling.Molecular cancer research : MCR · 2016Article
- IκBβ enhances the generation of the low-affinity NFκB/RelA homodimer.Nature communications · 2015Article
- Inhibition of Oncogenic Transcription Factor REL by the Natural Product Derivative Calafianin Monomer 101 Induces Proliferation Arrest and Apoptosis in Human B-Lymphoma Cell Lines.Molecules (Basel, Switzerland) · 2015Article
- NF-κB functions in tumor initiation by suppressing the surveillance of both innate and adaptive immune cells.Cell reports · 2014Article
- Analysis of the RelA:CBP/p300 interaction reveals its involvement in NF-κB-driven transcription.PLoS biology · 2013Article
- Inhibition of GSK3β-mediated BACE1 expression reduces Alzheimer-associated phenotypes.The Journal of clinical investigation · 2013Article
- Targeting of several glycolytic enzymes using RNA interference reveals aldolase affects cancer cell proliferation through a non-glycolytic mechanism.The Journal of biological chemistry · 2012Article
- Senescence and NFκB: A trojan horse in tumors?Oncoimmunology · 2012Article
- TRAF6 is an amplified oncogene bridging the RAS and NF-κB pathways in human lung cancer.The Journal of clinical investigation · 2011Article
- The role of RelA (p65) threonine 505 phosphorylation in the regulation of cell growth, survival, and migration.Molecular biology of the cell · 2011Article
- NF-κB controls energy homeostasis and metabolic adaptation by upregulating mitochondrial respiration.Nature cell biology · 2011Article
- The Differential Effect of Toxoplasma Gondii Infection on the Stability of BCL2-Family Members Involves Multiple Activities.Frontiers in microbiology · 2011Article
- High-throughput, single-cell NF-κB dynamics.Current opinion in genetics & development · 2010Review
- Downregulation of NF-kappaB signaling by mutant huntingtin proteins induces oxidative stress and cell death.Cellular and molecular life sciences : CMLS · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of the NF-kappaB pathway can either promote or block apoptosis and oncogenesis in different cell types and circumstances. In this report, we show that independently derived immortalized mouse embryonic fibroblast cell lines prepared from RelA knockout mice have different phenotypes, based on their sensitivity to tumor necrosis factor alpha (TNFalpha)-induced apoptosis, morphology, ability to form colonies in soft agar, and the presence of distinct kappaB site-binding complexes. In addition, these RelA-deficient cell lines appear to have distinct alterations in the p53 pathway, which correlate with the normal vs transformed status of individual cell lines. We have also infected mouse embryonic fibroblasts lacking RelA, c-Rel or p50 with a retrovirus for the expression of v-Ha-Ras to determine whether individual NF-kappaB family members are required for Ras-mediated transformation. All three NF-kappaB-deficient cell types could be transformed by v-Ha-Ras. However, v-Ras-infected RelA-deficient cells formed colonies in soft agar at an approximately fourfold reduced efficiency compared to v-Ras-transformed control mouse 3T3 and p50-deficient cells. Ras transformation did not alter the sensitivity of RelA-deficient cells to TNFalpha-induced apoptosis, and Ras transformation did not affect the general resistance of 3T3, c-Rel-deficient, and p50-deficient cells to TNFalpha-induced apoptosis. However, TNFalpha specifically and dose-dependently decreased the ability of v-Ras-transformed RelA-deficient cells to form colonies in soft agar. These results suggest that RelA is a potential protein target for human tumors driven by oncogenic Ras mutations, but caution that inhibition of RelA may promote tumorigenesis in some circumstances.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.