ArticleJournal of cellular biochemistry2009
Nit1 and Fhit tumor suppressor activities are additive.
Article in Journal of cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Nit1 is upregulated in non-small cell lung cancer and promotes cancer cell proliferation and invasion and regulates EMT-related molecules and cyclins.Journal of Cancer · 2025Article
- Review
- The Rosetta Stone Hypothesis-Based Interaction of the Tumor Suppressor Proteins Nit1 and Fhit.Cells · 2023Article
- NIT1 suppresses tumour proliferation by activating the TGFβ1-Smad2/3 signalling pathway in colorectal cancer.Cell death & disease · 2018Article
- Nit1 is a metabolite repair enzyme that hydrolyzes deaminated glutathione.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Clinical features and treatment of patients with esophageal cancer and a history of gastrectomy: a multicenter, questionnaire survey in Kyushu, Japan.Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus · 2016Article
- Reduction in squamous cell carcinomas in mouse skin by dietary zinc supplementation.Cancer medicine · 2016Article
- Nitrilase 1 modulates lung tumor progression in vitro and in vivo.Oncotarget · 2016Article
- A novel role for the tumour suppressor Nitrilase1 modulating the Wnt/β-catenin signalling pathway.Cell discovery · 2016Article
- Lipid Peroxide-Derived Short-Chain Carbonyls Mediate Hydrogen Peroxide-Induced and Salt-Induced Programmed Cell Death in Plants.Plant physiology · 2015Article
- Effect of zinc supplementation on N-nitrosomethylbenzylamine-induced forestomach tumor development and progression in tumor suppressor-deficient mouse strains.Carcinogenesis · 2011Article
- Hits, Fhits and Nits: beyond enzymatic function.Advances in enzyme regulation · 2011Review
- Common fragile site tumor suppressor genes and corresponding mouse models of cancer.Journal of biomedicine & biotechnology · 2011Review
- Fragile histidine triad protein: structure, function, and its association with tumorogenesis.Journal of cancer research and clinical oncology · 2010Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The fragile histidine triad gene (human FHIT, mouse Fhit) has been shown to act as a tumor suppressor gene. Nit1 and Fhit form a fusion protein, encoded by the NitFhit gene in flies and worms, suggesting that mammalian Nit1 and Fhit proteins, which are encoded by genes on different chromosomes in mammals, may function in the same signal pathway(s). A previous study showed that Nit1 deficiency in knockout mice confers a cancer prone phenotype, as does Fhit deficiency. We have now assessed the tumor susceptibility of Fhit(-/-)Nit1(-/-) mice and observed that double knockout mice develop more spontaneous and carcinogen-induced tumors than Fhit(-/-) mice, suggesting that the extent of tumor susceptibility due to Nit1 and Fhit deficiency is additive, and that Nit1 and Fhit affect distinct signal pathways in mammals. Nit1, like Fhit, is present in cytoplasm and mitochondria but not nuclei. Because Fhit deficiency affects responses to replicative and oxidative stress, we sought evidence for Nit1 function in response to such stresses in tissues and cultured cells: when treated with hydroxyurea, the normal kidney-derived double-deficient cells appear not to activate the pChk2 pathway and when treated with H(2)O(2), show little evidence of DNA damage, compared with wild type and Fhit(-/-) cells. The relevance of Nit1 deficiency to human cancers was examined in human esophageal cancer tissues, and loss of Nit1 expression was observed in 48% of esophageal adenocarcinomas.
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.