ArticleProceedings of the National Academy of Sciences of the United States of America2002
Restoration of fragile histidine triad (FHIT) expression induces apoptosis and suppresses tumorigenicity in lung and cervical cancer cell lines.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 161 citations in OpenAlex.
- Single-cell and Mendelian analyses reveal shared mechanisms between head and neck neoplasms and aging.Discover oncology · 2026Article
- Molecular and System-Level Characterization of MMP12 Suppression in Lung Cancer: A Combined Bioinformatics and Molecular Approach.International journal of molecular sciences · 2025Article
- Inhibition of GSK3β is synthetic lethal with FHIT loss in lung cancer by blocking homologous recombination repair.Experimental & molecular medicine · 2025Article
- Integrated analysis ofCell cycle (Georgetown, Tex.) · 2024Review
- Expression of Tumor SuppressorInternational journal of molecular sciences · 2023Article
- Germinal epimutation of Fragile Histidine Triad (FHIT) gene is associated with progression to acute and chronic adult T-cell leukemia diseases.Molecular cancer · 2021Article
- The fission yeast FHIT homolog affects checkpoint control of proliferation and is regulated by mitochondrial electron transport.Cell biology international · 2020Article
- Fhit-Fdxr interaction in the mitochondria: modulation of reactive oxygen species generation and apoptosis in cancer cells.Cell death & disease · 2019Article
- EPB41L3 is a potential tumor suppressor gene and prognostic indicator in esophageal squamous cell carcinoma.International journal of oncology · 2018Article
- NIT1 suppresses tumour proliferation by activating the TGFβ1-Smad2/3 signalling pathway in colorectal cancer.Cell death & disease · 2018Article
- Recent findings on epigenetic gene abnormalities involved in uterine cancer.Molecular and clinical oncology · 2017Article
- FHIT promoter DNA methylation and expression analysis in childhood acute lymphoblastic leukemia.Oncology letters · 2017Article
- Fhit, a tumor suppressor protein, induces autophagy via 14-3-3τ in non-small cell lung cancer cells.Oncotarget · 2017Article
- Synergism between RIZ1 gene therapy and paclitaxel in SiHa cervical cancer cells.Cancer gene therapy · 2016Article
- Association of activated Gαq to the tumor suppressor Fhit is enhanced by phospholipase Cβ.BMC cancer · 2015Article
- FHIT loss confers cisplatin resistance in lung cancer via the AKT/NF-κB/Slug-mediated PUMA reduction.Oncogene · 2015Article
- Anti-carcinogenic effects of the phenolic-rich extract from abnormal Savda Munziq in association with its cytotoxicity, apoptosis-inducing properties and telomerase activity in human cervical cancer cells (SiHa).BMC complementary and alternative medicine · 2015Article
- Genetic and Chromosomal Aberrations and Their Clinical Significance in Renal Neoplasms.BioMed research international · 2015Review
- Characterization of the role of Fhit in suppression of DNA damage.Advances in biological regulation · 2013Article
- LY294002 induces differentiation and inhibits invasion of glioblastoma cells by targeting GSK-3beta and MMP.EXCLI journal · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Loss of expression of the Fhit protein is often associated with the development of many human epithelial cancers, including lung and cervical carcinomas. Restoration of Fhit expression in cell lines derived from these tumors has however yielded conflicting results, prompting the need for careful evaluation of the oncosuppressive potential of FHIT. In the present study, we have investigated the effect of Fhit reintroduction in seven lung cancer and three cervical cancer cell lines. To achieve efficient gene transfer and high levels of transgene expression, we have used an adenoviral vector to transduce the FHIT gene. The induction of apoptosis was evaluated by using the terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling assay and propidium iodide staining. Activation of caspases was detected by using Western blot analysis, and tumorigenic potential of transduced cells in the nude mouse was also assessed. Restoration of Fhit expression induced apoptosis in all Fhit-negative cell lines, with Calu-1, H460, and A549 being the most susceptible among the lung cancer cell lines and SiHa cells among cervical carcinomas. Activation of caspase-8 was always associated with Fhit-mediated apoptosis, and in vivo tumorigenicity was either abolished by FHIT gene transfer (in H460 and SK-Mes cells) or strongly suppressed (in A549 and SiHa cells). Our data demonstrate oncosuppressive properties and strong proapoptotic activity of the Fhit protein in lung and cervical cancer cell lines and strengthens the hypothesis of its possible use as a therapeutic tool.
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