ArticleOncogene2005
TRAIL is a key target in S-phase slowing-dependent apoptosis induced by interferon-beta in cervical carcinoma cells.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- A combined antitumor strategy of separately transduced mesenchymal stem cells with soluble TRAIL and IFNβ produces a synergistic activity in the reduction of lymphoma and mice survival enlargement.Molecular medicine reports · 2022Article
- Prediction of signaling cross-talks contributing to acquired drug resistance in breast cancer cells by Bayesian statistical modeling.BMC systems biology · 2015Article
- IκΒα inhibits apoptosis at the outer mitochondrial membrane independently of NF-κB retention.The EMBO journal · 2014Article
- Nip the HPV encoded evil in the cancer bud: HPV reshapes TRAILs and signaling landscapes.Cancer cell international · 2013Article
- Type I interferons induce apoptosis by balancing cFLIP and caspase-8 independent of death ligands.Molecular and cellular biology · 2013Article
- Interferon-β produces synergistic combinatory anti-tumor effects with cisplatin or pemetrexed on mesothelioma cells.PloS one · 2013Article
- Interferons induce the expression of IFITM1 and IFITM3 and suppress the proliferation of rat neonatal cardiomyocytes.Journal of cellular biochemistry · 2012Article
- Article
- Cytokine-receptor interactions as drug targets.Current opinion in chemical biology · 2010Review
- Killing of human melanoma cells induced by activation of class I interferon-regulated signaling pathways via MDA-7/IL-24.Cytokine · 2008Article
- Cell cycle arrest and apoptosis induced by the coronavirus infectious bronchitis virus in the absence of p53.Virology · 2007Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN)-beta induces S-phase slowing and apoptosis in human papilloma virus (HPV)-positive cervical carcinoma cell line ME-180. Here, we show that apoptosis is a consequence of the S-phase lengthening imposed by IFN-beta, demonstrating the functional correlation between S-phase alteration and apoptosis induction. In ME-180 cells, where p53 function is inhibited by HPV E6 oncoprotein, IFN-beta effects on cell cycle and apoptosis occur independently of p53. The apoptosis due to IFN-beta is mediated by the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in a manner dependent on the S-phase deregulation. IFN-beta appears to increase TRAIL expression both directly at the mRNA level and indirectly by augmenting surface protein levels as a consequence of the induced S-phase cell accumulation. Moreover, the alteration of the S-phase due to IFN-beta promotes TRAIL-dependent apoptosis by potentiating cell sensitivity to TRAIL, possibly through induction of a proapoptotic NF-kappaB activity and TRAIL-R2 receptor expression. Interestingly, IFN-beta-induced TRAIL-dependent apoptotic events strongly differ in the requirement of caspase activity. These results show that IFN-beta may induce an apoptotic response by deregulating cell cycle. Understanding the linkage between these mechanisms appears to be of primary importance in the search for new IFN-based therapeutic strategies to circumvent cancer disease or improve clinical outcome.
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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.