ArticlePloS one2012
FLASH knockdown sensitizes cells to Fas-mediated apoptosis via down-regulation of the anti-apoptotic proteins, MCL-1 and Cflip short.
Article in PloS one, 2012. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Optimizing Recombinant Protein Production in CHO Cells by Silencing the Caspase 8 Associated Protein 2 Gene via the CRISPR-Cas9 System.Molecular biotechnology · 2026Article
- Dual role of CASP8AP2/FLASH in regulating epithelial-to-mesenchymal transition plasticity (EMP).Translational oncology · 2024Article
- Low miR-210 andOncology letters · 2017Article
- Genome-wide screen of cell-cycle regulators in normal and tumor cells identifies a differential response to nucleosome depletion.Cell cycle (Georgetown, Tex.) · 2017Article
- FLASH protects ZEB1 from degradation and supports cancer cells' epithelial-to-mesenchymal transition.Oncogenesis · 2016Article
- Overexpression of WDR79 in non-small cell lung cancer is linked to tumour progression.Journal of cellular and molecular medicine · 2016Article
- Nuclear Compartmentalization of Serine Racemase Regulates D-Serine Production: IMPLICATIONS FOR N-METHYL-D-ASPARTATE (NMDA) RECEPTOR ACTIVATION.The Journal of biological chemistry · 2015Article
- Role of the nucleus in apoptosis: signaling and execution.Cellular and molecular life sciences : CMLS · 2015Review
- FLASH/casp8ap2 is indispensable for early embryogenesis but dispensable for proliferation and differentiation of ES cells.PloS one · 2014Article
- SUMO regulates proteasome-dependent degradation of FLASH/Casp8AP2.Cell cycle (Georgetown, Tex.) · 2013Article
- Cetuximab-siRNA Conjugate Linked Through Cationized Gelatin Knocks Down KRAS G12C Mutation in NSCLC Sensitizing the Cells Toward Gefitinib.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
FLASH (FLICE-associated huge protein or CASP8AP2) is a large multifunctional protein that is involved in many cellular processes associated with cell death and survival. It has been reported to promote apoptosis, but we show here that depletion of FLASH in HT1080 cells by siRNA interference can also accelerate the process. As shown previously, depletion of FLASH halts growth by down-regulating histone biosynthesis and arrests the cell cycle in S-phase. FLASH knockdown followed by stimulating the cells with Fas ligand or anti-Fas antibodies was found to be associated with a more rapid cleavage of PARP, accelerated activation of caspase-8 and the executioner caspase-3 and rapid progression to cellular disintegration. As is the case for most anti-apoptotic proteins, FLASH was degraded soon after the onset of apoptosis. Depletion of FLASH also resulted in the reduced intracellular levels of the anti-apoptotic proteins, MCL-1 and the short isoform of cFLIP. FLASH knockdown in HT1080 mutant cells defective in p53 did not significantly accelerate Fas mediated apoptosis indicating that the effect was dependent on functional p53. Collectively, these results suggest that under some circumstances, FLASH suppresses apoptosis.
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