ArticleThe Journal of biological chemistry2008
Fhit interaction with ferredoxin reductase triggers generation of reactive oxygen species and apoptosis of cancer cells.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 3 syntheses or guidelines pooled it, 68 citations in OpenAlex.
- The clinicopathological significance of FHIT hypermethylation in non-small cell lung cancer, a meta-analysis and literature review.Scientific reports · 2016Pooled it
- The clinicopathological significance and ethnic difference of FHIT hypermethylation in non-small-cell lung carcinoma: a meta-analysis and literature review.Drug design, development and therapy · 2016Pooled it
- The clinicopathological significance and drug target potential of FHIT in breast cancer, a meta-analysis and literature review.Drug design, development and therapy · 2015Pooled it
- Review
- Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases.International review of cell and molecular biology · 2018Review
- Ferredoxin reductase is critical for p53-dependent tumor suppression via iron regulatory protein 2.Genes & development · 2017Article
- Fhit, a tumor suppressor protein, induces autophagy via 14-3-3τ in non-small cell lung cancer cells.Oncotarget · 2017Article
- Identification of Fhit as a post-transcriptional effector of Thymidine Kinase 1 expression.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017Article
- Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response.PLoS genetics · 2016Review
- Article
- Determining crystal structures through crowdsourcing and coursework.Nature communications · 2016Article
- A Fhit-mimetic peptide suppresses annexin A4-mediated chemoresistance to paclitaxel in lung cancer cells.Oncotarget · 2016Article
- Association of activated Gαq to the tumor suppressor Fhit is enhanced by phospholipase Cβ.BMC cancer · 2015Article
- Tumor Suppressor WWOX Contributes to the Elimination of Tumorigenic Cells in Drosophila melanogaster.PloS one · 2015Article
- The FHIT gene product: tumor suppressor and genome "caretaker".Cellular and molecular life sciences : CMLS · 2014Review
- Very large common fragile site genes and their potential role in cancer development.Cellular and molecular life sciences : CMLS · 2014Review
- Replicative Stress and the FHIT Gene: Roles in Tumor Suppression, Genome Stability and Prevention of Carcinogenesis.Cancers · 2014Article
- A knockdown with smoke model reveals FHIT as a repressor of Heme oxygenase 1.Cell cycle (Georgetown, Tex.) · 2014Article
- Activation state-dependent interaction between Gαq subunits and the Fhit tumor suppressor.Cell communication and signaling : CCS · 2013Article
- The roles of sphingosine kinases 1 and 2 in regulating the Warburg effect in prostate cancer cells.Cellular signalling · 2013Article
Corrections and comments
- Retraction · 2017-08-03Error in Image · · see also https://www.nytimes.com/2017/03/08/science/cancer-carlo-croce.html?hp&action=click&pgtype=Homepage&clickSource=image&module=photo-spot-region®ion=top-news&WT.nav=top-news&_r=2
- Retracted
Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Fhit protein is lost in most cancers, its restoration suppresses tumorigenicity, and virus-mediated FHIT gene therapy induces apoptosis and suppresses tumors in preclinical models. We have used protein cross-linking and proteomics methods to characterize a Fhit protein complex involved in triggering Fhit-mediated apoptosis. The complex includes Hsp60 and Hsp10 that mediate Fhit stability and may affect import into mitochondria, where it interacts with ferredoxin reductase, responsible for transferring electrons from NADPH to cytochrome P450 via ferredoxin. Viral-mediated Fhit restoration increases production of intracellular reactive oxygen species, followed by increased apoptosis of lung cancer cells under oxidative stress conditions; conversely, Fhit-negative cells escape apoptosis, carrying serious oxidative DNA damage that may contribute to an increased mutation rate. Characterization of Fhit interacting proteins has identified direct effectors of the Fhit-mediated apoptotic pathway that is lost in most cancers through loss of Fhit.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.