ArticleMechanisms of ageing and development2009
Chronic NF-kappaB activation delays RasV12-induced premature senescence of human fibroblasts by suppressing the DNA damage checkpoint response.
Article in Mechanisms of ageing and development, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- The IKKα-regulated microRNA miR-9-5p mediates lung cancer growth and invasiveness via CDH1/Wnt/β-catenin signalling.Cell death discovery · 2026Article
- Identification of Oncogene-Induced Senescence-Associated MicroRNAs.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Sustained activation of NF-κB through constitutively active IKKβ leads to senescence bypass in murine dermal fibroblasts.Cell cycle (Georgetown, Tex.) · 2024Article
- An Expanded Interplay Network between NF-κB p65 (RelA) and E2F1 Transcription Factors: Roles in Physiology and Pathology.Cancers · 2022Article
- The Influence of Oncogenic RAS on Chemotherapy and Radiotherapy Resistance Through DNA Repair Pathways.Frontiers in cell and developmental biology · 2022Review
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- Roles of NF-κB Signaling in the Regulation of miRNAs Impacting on Inflammation in Cancer.Biomedicines · 2018Review
- Construction of a computable network model for DNA damage, autophagy, cell death, and senescence.Bioinformatics and biology insights · 2013Article
- cIAP2 represses IKKα/β-mediated activation of MDM2 to prevent p53 degradation.Cell cycle (Georgetown, Tex.) · 2012Article
- The canonical NF-κB pathway differentially protects normal and human tumor cells from ROS-induced DNA damage.Cellular signalling · 2012Article
- The microenvironment in hepatocyte regeneration and function in rats with advanced cirrhosis.Hepatology (Baltimore, Md.) · 2012Article
- Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity.Genes & development · 2011Article
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Authors and funding
8 authors.
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Abstract
Normal cells divide for a limited number of generations, after which they enter a state of irreversible growth arrest termed replicative senescence. While replicative senescence is due to telomere erosion, normal human fibroblasts can undergo stress-induced senescence in response to oncogene activation, termed oncogene-induced senescence (OIS). Both, replicative and OIS, initiate a DNA damage checkpoint response (DDR) resulting in the activation of the p53-p21(Cip1/Waf1) pathway. However, while the nuclear factor-kappaB (NF-kappaB) signaling pathway has been implicated in DDR, its role in OIS has not been investigated. Here, we show that oncogenic Ha-RasV12 promoted premature senescence of IMR-90 normal human diploid fibroblasts by activating DDR, hence verifying the classical model of OIS. However, enforced expression of a constitutively active IKKbeta T-loop mutant protein (IKKbetaca), significantly delayed OIS of IMR-90 cells by suppressing Ha-RasV12 instigated DDR. Thus, our experiments have uncovered an important selective advantage in chronically activating canonical NF-kappaB signaling to overcome the anti-proliferative OIS response of normal primary human fibroblasts.
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