ReviewCancer science2009
Fragile gene product, Fhit, in oxidative and replicative stress responses.
Review in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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
24 citing papers in PubMed, 35 citations in OpenAlex.
- Genome-wide association study of lung function decline using elastic-net regression: a prospective analysis in Korean cohort.Human genomics · 2025Article
- Association of FHIT gene variant and salty food preference with the incidence of metabolic syndrome.Genes & nutrition · 2025Article
- Re-evaluation of Diadenosine Tetraphosphate (ApFrontiers in molecular biosciences · 2020Review
- Role of HSP60/HSP10 in Lung Cancer: Simple Biomarkers or Leading Actors?Journal of oncology · 2020Review
- Fhit-Fdxr interaction in the mitochondria: modulation of reactive oxygen species generation and apoptosis in cancer cells.Cell death & disease · 2019Article
- Impact of FHIT loss on the translation of cancer-associated mRNAs.Molecular cancer · 2017Article
- Acetylation of hMOF Modulates H4K16ac to Regulate DNA Repair Genes in Response to Oxidative Stress.International journal of biological sciences · 2017Article
- Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response.PLoS genetics · 2016Review
- Fhit loss-associated initiation and progression of neoplasia in vitro.Cancer science · 2016Article
- Correlation of Aurora-A expression with the effect of chemoradiation therapy on esophageal squamous cell carcinoma.BMC cancer · 2015Article
- The FHIT gene product: tumor suppressor and genome "caretaker".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
- Article
- Stepwise activation of the ATR signaling pathway upon increasing replication stress impacts fragile site integrity.PLoS genetics · 2013Article
- Characterization of the role of Fhit in suppression of DNA damage.Advances in biological regulation · 2013Article
- microRNA-based cancer cell reprogramming technology.Experimental and therapeutic medicine · 2012Article
- Drosophila orthologue of WWOX, the chromosomal fragile site FRA16D tumour suppressor gene, functions in aerobic metabolism and regulates reactive oxygen species.Human molecular genetics · 2011Article
- Hits, Fhits and Nits: beyond enzymatic function.Advances in enzyme regulation · 2011Review
- Genome-wide assessment for genetic variants associated with ventricular dysfunction after primary coronary artery bypass graft surgery.PloS one · 2011Article
- Disruption of HOX activity leads to cell death that can be enhanced by the interference of iron uptake in malignant B cells.Leukemia · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Though the fragile histidine triad gene product, Fhit, was discovered and characterized as a tumor suppressor 13 years ago, its sequence, structure, and cellular location did not provide clues to aid discovery of its mechanisms of suppression. Recently, using chemical cross-linkers and immunoprecipitation, a Fhit protein complex was identified that includes Hsp60 and Hsp10 which may mediate Fhit stability and mitochondrial localization, where Fhit binds and stabilizes ferredoxin reductase (Fdxr); when Fdxr is overexpressed, it can lead to production of reactive oxygen species (ROS) that induce apoptosis. Cancer cells expressing endogenous or exogenous Fhit, when exposed to H(2)O(2), an oxidative stress, produce higher levels of apoptosis-inducing ROS than matched, Fhit-negative cells; the Fhit-negative cancer cells survive, carrying DNA damage. In addition to this mitochondrial function, Fhit-overexpression in cancer cells exposed to replicative stress-inducing agents leads to enhanced caspase 3 activation and apoptosis, due to defective Chk1 activation. Thus, damage to the fragile FHIT locus leads to reduced expression of Fhit protein, and makes a two-pronged contribution to development of preneoplastic clonal expansion: (1) absence or reduction of Fhit leads to reduced expression of Fdxr and reduced ROS-induced apoptosis; (2) cells that escape ROS- or replicative stress-induced apoptosis can carry misrepaired DNA damage. The aberrant DNA damage response checkpoint in Fhit-deficient preneoplasias and cancers may make these lesions targets for inhibitors of proteins such as Parp1 and Chk1 with important roles in checkpoint responses, as observed for BRCA1-deficient cancer cells that also exhibit DNA damage repair deficiencies.
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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.